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Vasotec

Vasotec is an effective strong preparation which is taken in treatment of diabetes symptoms as hypertension diseases, kidney problems, and congestive heart failure. Vasotec can be also helpful for patients after heart attack. Vasotec operates by reducing blood pressure and regulating blood provision to the heart.

Other names for this medication:

Similar Products:
Lotensin, Capoten, Monopril, Prinivil, Zestril, Univasc, Aceon, Accupril, Altace, Mavik

 

Also known as:  Enalapril.

Description

Vasotec is created by pharmacy specialists to combat not also diabetes symptoms as hypertension diseases, kidney problems, and congestive heart failure but it can be helpful for patients after heart attack.

Target of Vasotec is to control and decrease level of blood pressure.

Vasotec is also known as Enalapril, Renitec, BQL, Benalipril, Amprace, Alphapril, Converten, Enalagamma, Enatec, Envas, Invoril, Xanef.

Vasotec operates by reducing blood pressure and regulating blood provision to the heart.

Vasotec can be used in combination with medicines for heart failure treatment.

Vasotec is ACE (angiotensin-converting enzyme) inhibitor.

Generic name of Vasotec is Enalapril.

Brand name of Vasotec is Vasotec.

Dosage

You should take it by mouth with water.

It is better to take Vasotec once or twice a day at the same time with meals or without it.

If you want to achieve most effective results do not stop taking Vasotec suddenly.

Overdose

If you overdose Vasotec and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Vasotec overdosage: fainting, dizziness.

Storage

Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Vasotec are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Vasotec if you are allergic to Vasotec components.

Be very careful with Vasotec if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Vasotec usage in case of having angioedema, throat, heart disease, diabetes, hands, kidney disease, lower legs, lupus, scleroderma.

Be careful with Vasotec usage in case of taking diuretics; aspirin and other nonsteroidal anti-inflammatory medications (NSAIDs) as indomethacin (Indocin); potassium supplements; lithium (such as Eskalith, Lithobid).

Nimotop can be not safety for elderly people.

Avoid dehydration.

Be careful with great care in case you want to undergo an operation (dental or any other).

Do not use potassium supplements or salt substitutes.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Do not stop taking Vasotec suddenly.

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The aim of this study was to assess the sigmoid line of elasticity in the human aorta.

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Most preclinical trials are designed to identify potential torsadogenicity test only for surrogates of torsade de pointes, most commonly prolongation of the heart rate corrected QT interval (QTc). This study was conducted to determine which correction method best accounts for the effects of changes in the RR interval on the QT interval of conscious rabbits. This study was also conducted to validate the use of conscious, sling-trained rabbits to assess the QTc interval, and to evaluate the reliability and accuracy of this preparation in predicting drug-induced QTc prolongation in humans.

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The present study showed that when NPE occurs, a high lung AngII concentration was associated with an imbalance between ACE mRNA to ACE2 mRNA expression level. Activated local RAS in lung tissue resulted in lung injury. Enalaprilat treatment may attenuate lung injury by interventing local RAS in lung tissue with decreased ratio of ACE mRNA to ACE2 mRNA and lung AngII concentration. The result will be significant for the angiotensin converting enzyme inhibitor used in the theatment of NPE.

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A single-dose, single-blind, crossover study of vasodilator/angiotensin-converting enzyme (ACE) inhibitor interactions was carried out in 16 volunteers. Enalapril 20 mg and lisinopril 20 mg were administered either alone or in combination with hydralazine 25 mg. Co-administration of hydralazine significantly increased the area under the plasma concentration time curve (AUC) of lisinopril (AUC0-48 h 766.8 +/- 66.3 ng.h/ml (lisinopril) vs 1022.3 +/- 115.3 ng.h/ml (lisinopril + hydralazine)). This did not occur with enalaprilat (AUC 710.1 +/- 51.2 ng.h/ml (enalapril) vs 681.9 +/- 44.9 ng.h/ml (enalapril + hydralazine); mean +/- SEM). Urinary recovery of lisinopril showed a similar trend, but group differences did not achieve statistical significance despite comparable confidence intervals. Although hydralazine had no effect on the bioavailability of enalapril, significantly increased bioavailability was observed with lisinopril. This type of drug interaction is rare. The underlying mechanism is unclear, but may relate to increased absorption of lisinopril.

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The proteolytic degradation of the enkephalin-containing heptapeptide Tyr-Gly-Gly-Phe-Met-Arg-Phe (YGGFMRF) was investigated by incubating the peptide with synaptic membranes from mouse whole brain and characterizing the formed products. The degradation products were derivatized with 4-dimethylaminoazobenzene-4'-isothiocyanate and then analyzed by high pressure liquid chromatography and by amino-terminal analysis. The incubation of YGGFMRF with synaptic membranes yielded YGGFM and RF as the degradation products. The angiotensin-converting enzyme (ACE) inhibitors, MK-422 and captopril, potently inhibited the formation of YGGFM and RF with IC50 values of 8 nM and 95 nM, respectively. The "enkephalinase A" inhibitor, thiorphan, weakly inhibited this dipeptidyl carboxypeptidase activity with an IC50 greater than 1 microM. YGGFMRF, MK-422, captopril, and thiorphan all produced a dose-dependent analgesic response in the mouse hot plate test when administered intracerebroventricularly. However, when subanalgesic doses of inhibitors were co-administered with a subanalgesic dose of YGGFMRF, only the ACE inhibitors, MK-422 and captopril, potentiated the analgesic response of the peptide. These data provide in vitro and in vivo evidence that ACE is the primary enzyme involved in the proteolytic degradation of YGGFMRF in the mouse brain.

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Peripheral blood mononuclear cells (PBMNCs) were isolated by gradient centrifugation from 10 patients on regular hemodialysis and 7 healthy control volunteers. A colony assay of hematopoietic progenitors was performed using the methylcellulose culture system. PBMNCs of 1 or 2 x 10(5) were plated in a medium containing EPO with various concentrations of ACE inhibitors or AT1 receptor antagonist and incubated for 14 days. Colonies of BFU-E were counted under an inverted microscope.

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In the control group postoperative blood creatinine and urea levels were significantly higher and CLcr measurements were significantly lower than the preoperative values (p<0.05). These values did not change in the enalaprilat group. Mean arterial pressure was similar in both groups (p>0.05), but SVR was lower (p<0.05) and CVP was higher (p<0.05) in the enalaprilat group than in the control group. In the enalaprilat group postoperative CO measurements were higher than the preoperative values (p<0.05).

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The laminin concentration was higher in the cells than in the medium, where an increase of its content was observed under high-glucose conditions (p < 0.01). Fibronectin, found only in the medium, was not modified by the high glucose concentration. Following enalaprilat administration, the laminin concentration was decreased under high-glucose conditions, both in the cell and in the medium (p < 0.001), whereas the fibronectin concentration was increased under high-glucose conditions (p < 0.001). The mRNA expression of laminin and fibronectin under high-glucose conditions only slightly increased. Enalaprilat decreased the fibronectin mRNA synthesis dramatically (>50%, p < 0.0001) under high-glucose conditions.

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We have previously shown that angiotensin converting enzyme-inhibitor (ACE-I) improved colonic inflammation and apoptosis in a dextran sodium sulfate (DSS)-induced colitis model. This study attempted to determine whether ACE-I could prevent the development of colonic fibrosis.

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Central hemodynamics, systemic oxygenation, and hormonal regulation of circulation (plasma renin activity, plasma endothelin, atrial natriuretic peptide, norepinephrine, epinephrine, and vasopressin concentrations, serum angiotensin-converting enzyme activity, and serum levels of aldosterone) were assessed at baseline before enalaprilat infusion, and repeatedly over 2 hours after the infusion. Enalaprilat infusion (median dose, 2.0 mg; infusion time, 48 minutes) caused a significant decrease in pulmonary capillary wedge pressure (p = 0.004), lasting until the end of the 2 hours' follow-up. This coincided with inhibition of serum angiotensin-converting enzyme activity (p < 0.001), an increase in plasma renin activity (p = 0.022), and decreases in plasma endothelin (p = 0.035), atrial natriuretic peptide (p = 0.005), and serum aldosterone (p = 0.001) concentrations. Cardiac output, venous admixture, and oxygen delivery and consumption remained unchanged.

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To understand if an anomaly of BK metabolism is associated with these reactions, the metabolism of BK and des-Arg9-BK was studied in the sera of four patients who presented with a severe hypotensive transfusion reaction. Tests were performed in the absence and the presence of complete in vitro inhibition of angiotensin-converting enzyme (ACE) activity by enalaprilat.

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To explore whether advanced oxidation protein products (AOPP) can cause endothelial dysfunction in vitro, and whether captopril exerts beneficial effect on impaired endothelium-dependent relaxation induced by exogenous advanced oxidation protein products and to investigate the potential mechanisms. Both the Acetylcholine (ACh)-induced endothelium-dependent relaxation (EDR), sodium nitroprusside-induced endothelium-independent relaxation of aortic rings were measured by recording isometric tension after the rings were exposed to AOPP-BSA in the absence or presence of captopril to assess the injury effect of AOPP-BSA and the protective effect of captopril on the aortic endothelium, respectively. Co-incubation of aortic rings with AOPP-BSA (3 mmol/L) for 90 minutes resulted in a significant inhibition of EDR to ACh, but had no effects on endothelium-independent relaxation to SNP. After incubation of the rings in the co-presence of captopril (3 to 30 micromol/L) or enalaprilat (30 micromol/L) with AOPP-BSA (3 mmol/L) for 90 minutes, captopril significantly and enalaprilat only partly attenuated the inhibition of EDR induced by AOPP-BSA. This protective effect of captopril (30 micromol/L) was abolished by N-nitro-L-arginine methyl ester (10 micromol/L), an inhibitor of nitric oxide synthase. Furthermore, the superoxide anion scavenger superoxide dismutase (SOD, 200 U/mL), and the nitric oxide precursor L-arginine (3 mmol/L) also ameliorated the impaired EDR caused by AOPP-BSA. But D-arginine had no effect on the impaired EDR caused by AOPP-BSA. AOPP-BSA can trigger endothelial dysfunction and captopril can protect the endothelium against functional damage induced by AOPP-BSA in rat aorta, increase nitric oxide bioavailability. The mechanisms of endothelial dysfunction induced by AOPP-BSA may include the decrease of NO and the generation of oxygen-free radicals.

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William Greenlee, the founder and president of MedChem Discovery Consulting LLC, has over three decades of research experience in industry at Merck Research Laboratories and the Schering-Plough Research Institute. He has contributed to the advancement of 20 drug candidates into preclinical development, 11 of which have progressed into clinical studies. Dr Greenlee was a member of the team that discovered the marketed drugs Vasotec™ and Prinivil™, and has led research teams that discovered several drug candidates that are now in clinical trials. His achievements and significant contributions to the field have been recognized with the presentation of a number of local and national awards, including the Alfred Burger Award in Medicinal Chemistry from the American Chemical Society and the Pennsylvania Drug Discovery Institute Drug Discovery Award. He was inducted into the American Chemical Society Medicinal Chemistry Hall of Fame in 2006. Dr Greenlee was elected a Fellow of the American Association for the Advancement of Science in 2007 and an American Chemical Society Fellow in 2009.

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The angiotensin-converting enzyme (ACE) inhibitor enalapril is commonly used to treat pediatric hypertension. Because some children are unable to swallow tablets or require doses less than the lowest available enalapril tablet, an enalapril suspension was developed. This study examined the relative bioavailability of enalapril suspension (10 mg) (S) compared with 10-mg marketed VASOTEC tablets (T) in 16 healthy adult subjects. The geometric mean ratio (S/T) estimate of urinary recovery of free enalaprilat, the active moiety, was 0.92 (90% confidence interval (CI): 0.80, 1.07). Urinary recovery data indicate that approximately 50% of the dose was absorbed (50% recovered in urine as enalapril plus enalaprilat) with about 30% of the dose recovered as free enalaprilat for both S and T. The geometric mean ratios (S/T) of serum AUC and C(max) were 1.01 (90% CI: 0.90, 1.13) and 0.98 (90% CI: 0.83, 1.16), respectively. Suspension T(max) was slightly shorter (0.5 h) than that for tablet, but this difference is not clinically significant. Both formulations were well tolerated and there were no clinically significant adverse experiences. We conclude that the bioavailability of enalapril oral suspension 10-mg is similar to that of VASOTEC 10-mg tablet. Instructions for compounding enalapril are provided.

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The isolated vascular effects of intravenous administration of the angiotensin converting enzyme (ACE) inhibitor enalaprilat were investigated. Thirty male patients undergoing cardiopulmonary bypass (CPB) were studied. According to a randomized sequence, 0.04 mg kg-1 enalaprilat (low-dose, n = 10), 0.08 mg kg-1 (high-dose, n = 10) enalaprilat or saline solution as placebo (control group, n = 10) was given as an i.v. bolus during CPB. Changes in mean arterial pressure (MAP) and venous reservoir (RV) of the extracorporeal circulation were studied as indices of arterial resistance and venous capacitance. Mean arterial blood pressure (MAP) and peripheral vascular resistance (SVR) were significantly more reduced in the high-dose enalaprilat group (MAP: -36 mm Hg after 9 min; SVR: -836 dyn s cm-5) than in the low-dose group (MAP: -13 mm Hg after 10 min). Volume of the reservoir (RV) decreased in both enalaprilat treated groups indicating additional (dose-dependent) venous pooling effects of the substance (low-dose: -300 ml; high-dose: -520 ml; control group: -100 ml). Skin capillary blood flow measured by laser Doppler flowmetry (LDF) increased after injection of 0.04 mg kg-1 enalaprilat, whereas it decreased significantly when MAP fell markedly in patients treated with high-dose enalaprilat. I.v. enalaprilat had dose-dependent vasodilating properties in the arterial and venous vessel system indicating reduction in pre- and afterload. Microcirculation in both enalaprilat treated groups improved as long as reduction in blood pressure was not limited.

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The influence of 21-day administration of captopril and enalaprilat on barium chloride and adrenaline-induced experimental arrhythmias was assessed. The experiments were performed on rabbits. Arrhythmias were evoked by two alternative arrhythmogen doses. The patterns of disturbances, their frequency and duration were evaluated on the basis of ECG examination. Antiarrhythmic properties of angiotensin converting enzyme inhibitors administered for 21 days were also compared with their effects after single administration. The results were subjected to statistic analysis. On the basis of the obtained results we were able to establish that repeated administration of enalaprilat decreases the frequency of barium chloride- and adrenaline-induced arrhythmias. Repeated administration of captopril and enalaprilat shortened the duration of adrenaline- and barium chloride-induced arrhythmias. Long-term enalaprilat administration was much more effective in preventing arrhythmias than its single dose, it also proved to be more efficient than either single or repeated administration of captopril.

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The renin angiotensin aldosterone system (RAAS) is a paramount target for the pharmacological treatment of cardiovascular diseases. As modeling and simulation techniques are becoming increasingly utilized in cardiovascular research, our aim was to develop a physiology-based model that describes the effect of different drugs at different doses on the RAAS and integrates physiology-based description drug pharmacokinetics (PK). First, a basic RAAS model was developed in which equations for drug effects were included and missing parameters estimated. Next, a physiology-based PK model for enalapril and enalaprilat was developed and coupled to the RAAS model. Simulation of the effects of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aliskiren administration on angiotensins I and II did not reveal significant overestimation or underestimation. For all drugs, the error numerics were acceptable. The model also encompassed the PK of intravenous and oral enalapril and its conversion to enalaprilat. In summary, we report a physiology-based model for the interaction of the RAAS biomarkers angiotensin I and II with enalapril, benazepril, aliskiren, and losartan that allows for an adequate description of the RAAS response after single administration of the drugs. Such a comprehensive description may lead to a better understanding of the effects of pharmacological interventions in the RAAS.

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There is evidence that angiotensin II is synthesized by the proximal tubule and secreted into the tubular lumen. This study examined the functional significance of endogenously produced angiotensin II on proximal tubule transport in male Sprague-Dawley rats. Addition of 10(-11), 10(-8), and 10(-6) M angiotensin II to the lumen of proximal convoluted tubules perfused in vivo had no effect on the rate of fluid reabsorption. The absence of an effect of exogenous luminal angiotensin II could be due to its endogenous production and luminal secretion. Luminal 10(-8) M Dup 753 (an angiotensin II receptor antagonist) resulted in a 35% decrease in proximal tubule fluid reabsorption when compared to control (Jv = 1.64 +/- 0.12 nl/mm.min vs. 2.55 +/- 0.32 nl/mm.min, P < 0.05). Similarly, luminal 10(-4) M enalaprilat, an angiotensin converting enzyme inhibitor, decreased fluid reabsorption by 40% (Jv = 1.53 +/- 0.23 nl/mm.min vs. 2.55 +/- 0.32 nl/mm.min, P < 0.05). When 10(-11) or 10(-8) M exogenous angiotensin II was added to enalaprilat (10(-4) M) in the luminal perfusate, fluid reabsorption returned to its baseline rate (Jv = 2.78 +/- 0.35 nl/mm.min). Thus, addition of exogenous angiotensin II stimulates proximal tubule transport when endogenous production is inhibited. These experiments show that endogenously produced angiotensin II modulates fluid transport in the proximal tubule independent of systemic angiotensin II.

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The objective of the study was to determine if bradykinin-induced airway microvascular leakage in rats was altered by pretreatment of animals with enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), or phosphoramidon, an inhibitor of endopeptidase 24.11 (EP 24.11). We found that the intravascular infusion of bradykinin induced microvascular leakage of Evans blue dye in tracheal tissue (0.088 +/- 0.035 micrograms/mg tissue) that was significantly amplified by pretreatment with 3.27 mM enalaprilat (0.458 +/- 0.226 micrograms/mg tissue), but not by pretreatment with 10 mM phosphoramidon (0.082 +/- 0.0453 micrograms/mg tissue). Leakage in carinal tissue was also amplified by pretreatment with 3.27 mM enalaprilat (0.205 +/- 0.050 vs. 0.036 +/- 0.006 micrograms/mg tissue for bradykinin alone), whereas no amplification was observed in parenchymal tissue by pretreatment with either inhibitor. These findings indicate that in the rat, ACE, but not EP 24.11, modulates bradykinin-induced airway microvascular leakage following intravascular infusion of these agents.

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Enalaprilat did not increase total cardiac output but redistributed flow to the lower body, with a concomitant decrease in arterial oxygen saturation. It is difficult to increase cardiac output in patients with a BCPC and ACEI should be used with caution in those with borderline aortic saturations.

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Preglomerular responses to vasoactive agonists utilize calcium released from intracellular stores and activation of calcium influx pathways to elicit vasoconstriction. The current study was performed to determine the role of calcium release from intracellular stores on the afferent arteriolar response to increases in perfusion pressure. Experiments were performed, in vitro, using the blood perfused, juxtamedullary nephron technique combined with videomicroscopy. The response of afferent arterioles to 30 mm Hg increases in perfusion pressure was determined before and after depletion of intracellular calcium pools with a 10-minute preincubation with 1 micromol/L thapsigargin or 100 micromol/L cyclopiazonic acid. Afferent arteriolar diameter averaged 20.2+/-1.0 microm (n=19) at a control perfusion pressure of 100 mm Hg. Increasing perfusion pressure to 130 and 160 mm Hg reduced afferent caliber by 10.7+/-1.0% (P<.05 versus con) and by 24.7+/-1.6% (P<.05 versus diameter at 130 mm Hg); respectively. Thapsigargin significantly increased afferent diameter by 21+/-2% (n=6) at 100 mm Hg and prevented pressure-induced autoregulatory responses. Afferent diameter averaged 24.3+/-1.7, 24.5+/-1.8 and 24.3+/-1.8 microm at perfusion pressures of 100, 130 and 160 mm Hg; respectively. Cyclopiazonic acid treatment also inhibited autoregulatory behavior but did not alter resting vessel diameter. Afferent arteriolar diameter (n=6) averaged 21.4+/-1.9 microm at 100 mm Hg and 20.9+/-2.1 and 20.5+/-2.2 microm at 130 and 160 mm Hg; respectively. Additional studies were performed to assess the role of phospholipase C activity in pressure-mediated autoregulatory behavior of afferent arterioles. Step increases in perfusion pressure decreased afferent diameter by 10.7+/-3.8 and 21.7+/-4.1%; respectively. Administration of the phospholipase C inhibitor, U-73122, (5 micromoles/L) did not significantly alter baseline diameter but did attenuate the pressure-mediated vasoconstrictor response. Increasing perfusion pressure to 130 and 160 mm Hg reduced afferent diameter by only 6.5+/-1.5 and 10.0+/-2.0%; respectively. These data demonstrate that interruption of calcium mobilization with thapsigargin, cyclopiazonic acid, or phospholipase C inhibition markedly attenuates pressure-mediated afferent arteriolar vasoconstriction and suggests that autoregulatory adjustments in afferent arteriolar diameter involve calcium release from inositoltrisphosphate(IP3)-sensitive intracellular stores.

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EN blunted the rise in ischemic intracellular sodium, measured using MRS. With reperfusion, EN-treated hearts recovered 80% of their preischemic ventricular function, compared with negligible recover, in controls. These beneficial effects of EN were blocked when the bradykinin receptor antagonist, HOE 140, was coadministered with EN. HOE 140 also blocked EN-mediated attenuation of ischemic intracellular acidosis.

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Angiotensin-converting enzyme (ACE) inhibitors are established as first-line therapy in chronic heart failure (CHF). However, little is known about the dosage-plasma-level relationship of ACE inhibitors in CHF and its relation to drug-induced adverse effects. We investigated 45 patients (age 55 +/- 10 years) with stable CHF who presented with a maintenance dosage of enalapril of either 5 mg b.i.d. (E10, n = 16), 10 mg b.i.d. (E20, n = 18), or 20 mg b.i.d. (E40, n = 11). This dosage was changed three times to treat all patients with lower, higher, and, finally, the initial dosage for 4 weeks each. Patients were examined clinically, by questionnaire, and by spiroergometry. In addition, neurohormones (atrial and brain natriuretic peptide and norepinephrine), enalaprilat trough levels, and serum potassium and creatinine were measured. Enalaprilat trough levels differed significantly between the three groups at study entry but also varied markedly within each group. In addition to the dose of enalapril, serum creatinine, severity of CHF, basal metabolic rate, and body weight significantly influenced enalaprilat trough levels (R2 =.84, p <.001). Within-patient comparisons revealed that serum creatinine (107 +/- 26 versus 102 +/- 20 micromol/liter) and potassium (3.8 +/- 0.4 versus 3.7 +/- 0. 3mmol/liter) were higher, cough was more common (scored on a scale of 0-8: 1.7 +/- 2.1 versus 1.4 +/- 1.8), and blood pressure was lower (systolic, 112 +/- 14 versus 117 +/- 13 mm Hg; diastolic, 66 +/- 9 versus 69 +/- 11 mm Hg) on the highest than on the lowest enalaprilat trough level (all p <.05). Highly variable enalaprilat trough levels and the fact that adverse effects were more common on high enalaprilat trough levels provide a rationale for individually adjusting ACE-inhibitor dose in case of adverse effects.

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The role played by several vasoactive mediators that are synthesized and released by the pulmonary vascular endothelium in the regulation of hypoxic pulmonary vasoconstriction (HPV) remains unclear. As a potent vasoconstrictor, angiotensin II could be involved. We tested the hypothesis that angiotensin-converting enzyme inhibition by enalaprilat and type 1 angiotensin II receptor blockade by candesartan would inhibit HPV.

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A placebo-controlled, randomized, double-blind protocol.

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To evaluate the effects of bilateral ureteral obstruction (BUO) on the levels of G-protein subunits in glomeruli, we examined the types and amounts of G-protein subunits in glomerular membranes from sham-operated control (SOC) rats and rats with BUO of 24 hours duration utilizing bacterial toxin-catalyzed ADP-ribosylation and specific antibodies. ADP-ribosylation catalyzed by cholera or pertussis toxin demonstrated the presence of Gs and Gi proteins in glomerular membranes. Immunoblots further revealed the existence of two types of G alpha s (45 and 52 kDa), as well as G alpha i2 (40 kDa), G alpha i3 (41 kDa), G alpha q/11 (42 kDa) and G beta (35 to 36 kDa) in glomerular membranes. The predominant subspecies of G alpha s was the 52 kDa protein. Detectable amounts of G alpha o were not found in glomerular membranes. Moreover, G-protein subunits were not detected in cytosolic extracts of glomeruli. Both forms of G alpha s and G alpha q/11 were significantly reduced in glomerular membranes from rats with BUO when compared to SOC rats. No significant difference in total G alpha i, G alpha i2 and G alpha i3 and G beta content was observed between the two groups of rats. In vivo pretreatment of rats with simultaneous administration of the angiotensin-converting enzyme inhibitor, enalaprilat, and the thromboxane synthase inhibitor, OKY-046, maintained the amount of G alpha s and G alpha q/11 in rats with BUO at the levels seen in SOC rats. The two drugs did not affect the amounts of G-protein subunits in glomerular membranes of SOC rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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The hydrolytic cleavage of angiotensin I has been studied in homogenate preparations of rat lung and aorta using gradient elution HPLC to monitor the formation of peptide products. Fresh crude homogenate preparations produced a rapid breakdown of angiotensin I to largely unidentifiable fragment peptides. Neither His-Leu nor angiotensin II was observed in these preparations even in the presence of captopril (20 microM) and the amino-peptidase inhibitors, puromycin, amastatin and bestatin. However, in freeze-thawed homogenates, angiotensin II and His-Leu were detectable together with the tetrapeptide, angiotensin (1-4). The addition of captopril (20 microM) reduced the amount of angiotensin II produced but did not completely block its formation. Higher concentrations of captopril or the addition of enalaprilat or EDTA did not further reduce the amount of angiotensin II produced. In the presence of captopril a peptide corresponding to des-Leu(10)angiotensin I was formed in relatively large amounts (equivalent to 40% of angiotensin I catabolized). Homogenates purified by concanavalin A affinity chromatography gave a clean hydrolysis of angiotensin I to angiotensin II and His-Leu which was completely blocked by captopril. These results suggest an ACE-like activity in rat lung and aorta that is not sensitive to converting enzyme inhibitors.

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The physical and chemical compatibility of enalaprilat in admixtures of dobutamine, dopamine, heparin, nitroglycerin, potassium chloride, or sodium nitroprusside, in 5% dextrose, were studied at room temperature over a 24-h period. Enalaprilat was found to be physically compatible and chemically stable in all admixture solutions tested.

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The rapid recognition and initiation of therapy are key to minimizing end-organ damage in patients with hypertensive emergency. Tailoring drug selection according to individual patient characteristics can optimize the management and potential outcomes of patients with hypertensive emergency.

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We have examined the effects of local intra-arterial infusion of enalaprilat (an angiotensin converting enzyme inhibitor) on responses initiated by concomitantly infused acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (a direct dilator of smooth muscle) in the forearm arterial beds of healthy volunteers. Although the angiotensin converting enzyme inhibitor alone did not affect basal forearm blood flow or vascular resistance, it significantly augmented the increase in blood flow and reduction in vascular resistance induced by acetylcholine (both p < 0.05). Coinfusion of enalaprilat did not enhance sodium nitroprusside-induced vasodilation. Pretreatment with NG-monomethyl-L-arginine blocked the augmentation of blood flow induced by the angiotensin converting enzyme inhibitor. The effect of enalaprilat was still observed after the administration of acetylsalicylic acid (p < 0.05). These results suggest that angiotensin converting enzyme inhibitors potentiate nonprostanoid endothelium-derived relaxing factor in normal human forearm vasculature.

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We measured changes in heart rate and lumbar sympathetic nerve activity in conscious, spontaneously hypertensive and Wistar-Kyoto rats during acute blood pressure lowering with nicardipine, enalaprilat and concomitant nicardipine/enalaprilat administration. In a buy vasotec second experiment, we determined the effect of these drugs on arterial baroreflex control of lumbar sympathetic nerve activity.

vasotec generic 2017-12-28

The area under the plasma concentration-time curve from 0 h to infinity (AUC0-∞) of active enalaprilat was 20% lower in subjects with the CES1 c.428G/A genotype than in those with the c.428G/G genotype (95% confidence interval of geometric mean ratio 0.64, 1.00; P = 0.049). The amount of enalaprilat excreted into the urine was 35% smaller in subjects with the CES1 c.428G/A genotype than in those with the c.428G/G genotype (P = 0.044). The CES1 genotype had no buy vasotec significant effect on the enalaprilat to enalapril AUC0-∞ ratio or on any other pharmacokinetic or pharmacodynamic parameters of enalapril or enalaprilat. The CES1 genotype had no significant effect on the pharmacokinetic or pharmacodynamic parameters of quinapril.

vasotec online 2017-06-03

This buy vasotec study was performed to determine whether acute inhibition of angiotensin-converting enzyme restores impaired endothelium-dependent vasorelaxation in patients with chronic heart failure.

vasotec generic equivalent 2016-06-21

Inhibition of the metallopeptidase neutral endopeptidase 3.4.24.11 (NEP) protects endogenous natriuretic peptides and potentiates their vasodepressor effects. Inhibition of angiotensin converting enzyme (ACE) attenuates the formation of angiotensin II and enhances the vasodepressor effect of endogenous kinins. A combination of NEP inhibition and ACE inhibition can potentially interact to shift the balance of vasoactive peptides toward vasodilation. This potential interaction was examined in conscious cardiomyopathic hamsters with low cardiac output and compensated heart failure. Neither the selective NEP inhibitor SQ 28,603 nor the selective ACE inhibitor enalaprilat (each at 30 mumol/kg, i.v.) caused significant changes in left ventricular end diastolic pressure or left ventricular systolic pressure when administered separately. However, the combination of these inhibitors, each at that dose, caused significant peak decreases in left ventricular end diastolic pressure and left ventricular systolic pressure buy vasotec of -12 +/- 1 and -18 +/- 4 mm Hg, respectively. In separate cardiomyopathic hamsters, this same combination of treatments resulted in significant decreases in mean arterial pressure (-13%) and total peripheral resistance (-37%) and an increase in cardiac output (36%) as compared with vehicle effects (P < .05). At 90 min after administration of SQ 28,603 alone, plasma atrial natriuretic peptide concentration was double that in the vehicle group. In the group receiving the combination of inhibitors, plasma atrial natriuretic peptide at 90 min was maintained at the high basal levels associated with this model despite the decrease in cardiac filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

vasotec tab 10mg 2015-08-10

All agents in the current study, with the exception buy vasotec of enalaprilat, dilated the IMA segments pre-contracted with U46619. Only GTN and SNP induced a complete (90-100%) relaxation. The order of efficacy of the in vitro relaxation was as follows: SNP, GTN, nicardipine, nicorandil, fenoldopam, hydralazine, adenosine, and labetalol. The potency was in the order of GTN, SNP, fenoldopam, nicorandil, hydralazine, adenosine, and nicardipine.

vasotec maximum dose 2015-12-28

1. To evaluate the effects of angiotensin-converting enzyme (ACE) inhibition on sympathetic nerve activity, renal and total norepinephrine (NE) spillover rates were examined under control conditions and during enalaprilat infusion at rest and in response to sodium nitroprusside (SNP)-induced hypotension. 2. Resting renal and total NE spillover rate during enalaprilat infusion were similar to control values. 3. During SNP infusion at 10 micrograms/kg per min, renal NE spillover rate increased by 26% in enalaprilat-treated group and by 39% in controls, in response to falls in mean arterial pressure (MAP) of 25 and 19% respectively. 4 buy vasotec . During sympathetic stimulation induced by SNP, total NE spillover rate was significantly increased in both groups, but the 50% (s.e.m. = 12) increase in the enalaprilat-treated group was less (P less than 0.05) than the 97% (s.e.m. = 16) change observed in controls. 5. Enalaprilat treatment resulted in a higher renal to total NE spillover ratio (P less than 0.05). The ratio fell in parallel in both groups during SNP-induced hypotension. 6. This study indicates that the sympathetic nervous system interacts dynamically with the renin-angiotensin system during hypotensive stimulation but this occurs predominantly at sites other than the kidney.

vasotec 50 mg 2017-11-30

The circulating and urinary bladder tissue concentrations of angiotensin I (ANG I) and angiotensin II [ANG-(1-8)] were examined in anesthetized Sprague-Dawley male rats given an intravenous bolus infusion of either ANG I, the angiotensin-converting enzyme (ACE) inhibitors enalaprilat or ramiprilat, or saline. The mean concentrations of ANG I and ANG-(1-8) were markedly higher in the urinary bladder tissue than in whole blood. There was a significant increase in the concentration of ANG I and ANG-(1-8), both in the urinary bladder tissue and the circulation, after the ANG I infusion. Both ACE inhibitors were associated with an increase in the concentration of whole blood ANG I; however, tissue ANG I levels were significantly increased only following ACE inhibition with ramiprilat but not with enalaprilat. Both plasma and urinary bladder tissue ANG-(1-8) levels decreased significantly buy vasotec following ACE inhibition, but only with ramiprilat. The elevated urinary bladder tissue levels of ANG I and ANG-(1-8) at baseline, compared with circulating levels, and the maintenance of ANG-(1-8) in bladder tissue in the face of inhibition of the circulatory renin-angiotensin system with enalaprilat support the presence of an autocrine/paracrine renin-angiotensin system in the urinary bladder. Under the current experimental conditions, ramiprilat appears to have enhanced bladder activity compared with enalaprilat.

vasotec 5 mg 2016-05-31

Experimental acute ischemic heart failure was induced in 19 splenectomized dogs by microsphere embolization of the left main coronary artery. Embolization was repeated until left ventricular end-diastolic pressure (LVEDP) reached 20 mm Hg and cardiac output decreased by 50%. The splanchnic vascular pressure-volume relation was determined by radionuclide plethysmography during the control stage, after acute buy vasotec heart failure had been established, and after administration of a vasodilator (hydralazine, enalaprilat, or nitroglycerin) at a dose sufficient to reduce mean aortic pressure by approximately 20%. Induction of acute heart failure was associated with a decrease in the splanchnic vascular volume from 100% to 86 +/- 2% and an increase in LVEDP from 6 +/- 1 to 21 +/- 1 mm Hg (P < .001). There was a parallel leftward shift of the splanchnic vascular pressure-volume curve. After the administration of hydralazine, enalaprilat, and nitroglycerin, the splanchnic vascular volumes increased from 86% to 88 +/- 3%, 96 +/- 3%, and 113 +/- 3%, respectively (P = NS, P < .01, and P < .001, respectively, versus heart failure). After drug administration, the LVEDPs were 18 +/- 2, 16 +/- 1, and 13 +/- 1 mm Hg (P = NS, P < .05, and P < .001, respectively, versus heart failure).

vasotec brand name 2016-12-27

In the ischemic myocardium, reperfusion is necessary for the salvage of cells and cardiac function. However, reperfusion itself causes 'reperfusion injury', leading to the damage of myocardial cells. This is reduced by several interventions, as measured by the limitation of infarct size or reduction of arrhythmias. Pharmacological agents that protect against injury include Na(+)/H(+) exchanger inhibitors, antioxidants, calcium antagonists, renin-angiotensin system antagonists and adenosine. N-acetylcysteine, diltiazem, verapamil, enalaprilat and adenosine have all showed promising results in patients with acute myocardial infarction when given before reperfusion. Cariporide was buy vasotec beneficial when added to cardioplegia. However, their use in daily practice awaits results from large clinical trials.

vasotec generic name 2016-12-05

SBR leads to significant intestinal hypertrophy. The addition of ACE-I to SBS rat resulted in a significant decline in ECs apoptosis. ACE mRNA expression was significantly buy vasotec elevated after SBS creation (0.24 ± 0.07 vs. 0.42 ± 0.11), and ACE-I administration further increased mucosal ACE mRNA expression (0.54 ± 0.12). Interestingly, AT1R mRNA expression showed a significant decline in the SBS group compared to Sham levels, and ACE-I administration increased AT1R mRNA expression to Sham levels. No significant difference in AT2R mRNA expression was found between Sham and SBS group.

vasotec medication 2015-09-25

The in vitro blood-perfused juxtamedullary nephron technique was utilized to determine the contribution of endothelium-derived relaxing factor (EDRF) to resting renal arteriolar caliber and to evaluate the interaction between EDRF and angiotensin II (ANG II) in renal microvascular control. Video microscopy was employed to visualize rat afferent and efferent arterioles and to measure their responses to blockade of nitric oxide (NO), which has been shown to account for much of the biological action of EDRF. The NO synthesis inhibitor, N omega-nitro-L-arginine (L-NNA), elicited vasoconstriction in a concentration-dependent manner, with 1,000 microM L-NNA significantly reducing both afferent (16 +/- 3%) and efferent (13 +/- 1%) diameters. This concentration of L-NNA also blocked the vasodilator response to 10 microM acetylcholine, while responsiveness to sodium nitroprusside was maintained. Vasoconstrictor responses to 1,000 microM L-NNA were attenuated in kidneys from rats pretreated with enalaprilat or losartan, reducing afferent diameter by 7 +/- 1 (n = 8) and 3 +/- 1% (n = 10) of control, respectively. Efferent arteriolar responses to L-NNA were similarly attenuated by losartan. The constrictor response to 10 nM ANG II was not exaggerated by L-NNA, suggesting that ANG II does not stimulate EDRF synthesis. These observations indicate that EDRF is continuously released in a quantity sufficient to affect both afferent and efferent arterioles of buy vasotec juxtamedullary nephrons in vitro. Furthermore, ANG II blockade attenuates the vasoconstriction elicited by L-NNA, suggesting that EDRF interacts with the renin-angiotensin system to control juxtamedullary afferent and efferent arteriolar resistance.

vasotec to buy 2016-09-26

1. Trandolaprilat was found to inhibit angiotensin I (Ang I)-induced contraction of the rat thoracic aorta, and to augment bradykinin(BK)-induced contraction of the guinea pig ileum. In inhibitory activity (IC50) on the Ang I induced contraction of the rat thoracic aorta, trandolaprilat was about 2.4 times as potent as enalaprilat. Concerning the augmenting activity (AC50) on bradykinin-induced contraction of the guinea pig ileum, the activity of trandolaprilat was similar to that of enalaprilat. 2. Trandolaprilat had no effect on contractions induced by norepinephrine, PGF2 alpha, 5-HT or CaCl2 in the thoracic aorta of rats. 3. Trandolaprilat produced endothelium-dependent relaxation. This relaxation was inhibited by NG-methyl-L buy vasotec -arginine treatment, suggesting that endothelium-dependent relaxation of trandolaprilat is related to endothelium-derived-relaxation-factor(EDRF/NO). Like trandolaprilat, captopril also produced endothelium-dependent relaxation, whereas enalaprilat had no effect.

vasotec dosage 2016-11-14

Experiments were Elavil Medication Sleep performed to determine the effect of a chloride channel blocker (indanyloxyacetic acid, IAA-94) on renal arteriolar vasoconstrictor responses to angiotensin II (AngII). The in vitro blood-perfused juxtamedullary nephron technique was exploited to provide access to the renal microvasculature of enalaprilat-treated rats. Under control conditions, 1 to 100 nmol/L AngII evoked concentration-dependent afferent arteriolar vasoconstriction. Baseline diameter of afferent arterioles was not altered by 30 mumol/L IAA-94; however, AngII responsiveness was markedly attenuated. The afferent response to K-induced depolarization was sustained in the presence of IAA-94. In efferent arterioles, neither baseline diameter nor AngII responsiveness was altered by IAA-94. These results suggest that full expression AngII-induced afferent (but not efferent) arteriolar vasoconstriction requires participation of chloride channels, which likely engender depolarization and subsequent opening of voltage-gated calcium channels.

vasotec 10mg tablet 2017-11-13

Randomized, single-blind, Aggrenox Overdose placebo-controlled trial.

vasotec usual dosage 2015-09-09

Our data indicate that stimulation of local kinin formation by use of a precursor for kinin formation or inhibition of kinin degradation by use of ACE inhibitors increases NO formation and is important in the control of cardiac O2 consumption. Vasodilation and control of myocardial O2 consumption Uroxatral Tab 10mg by NO may contribute importantly to the therapeutic actions of ACE inhibitors in cardiac disease states.

vasotec generic cost 2016-02-28

This was a placebo-controlled, randomized, double-blind study performed in 20 congestive heart failure patients (New York Heart Association class III or IV). Systemic and regional hemodynamic parameters, biological parameters, and blood gases were measured before and repeatedly after the onset of infusion. Compared with placebo, enalaprilat decreased pulmonary capillary wedge pressure (-37% versus -10%, P = .001), diastolic and mean systemic blood pressures (-21% versus 0%, P = .009, and -18% versus -1%, P = .026, respectively), diastolic and mean pulmonary blood pressures (-21% versus -8%, P = .040; -18% versus -9%, P = .046), and brachial and renal resistances (-44% versus -14%, P = .017, and -22% versus -2%, P = .014, respectively); increased brachial and renal blood flows (+77% versus +8%, P = .036, and +12% versus 0%, P = .043, respectively), arterial oxygen tension (+2% versus -16%, P = .041), and arterial oxygen saturation (+1% versus -2%, P = .045); and tended to decrease rate-pressure product (-19% versus -7%, P = .076), increase brachial artery diameter (+13% versus 0%, P = .081), and improve intrapulmonary shunt (-18% versus +16%, P = .080). Enalaprilat did not affect cardiac output or carotid or hepatosplanchnic Suprax Pediatric Dosage hemodynamics.

vasotec review 2017-09-05

The Zithromax 250 Dosage proliferating cell nuclear antigen labeling index was higher in the lisinopril-treated group than in the control group at all time points after hepatectomy, except 120 hours. The remnant liver dry weight was higher in lisinopril-treated rats than in control rats at early time points after surgery. The liver DNA content was higher in three angiotensin-converting enzyme inhibitor-treated groups than in the control group at 36 hours after hepatectomy. The bradykinin-induced regenerative response was similar to the lisinopril-induced response, and losartan induced a lower hepatocyte labeling index in comparison to the control group at 36 hours after hepatectomy.

vasotec reviews 2015-12-29

In vessels pre-contracted with phenylephrine or KCl, thiopental-induced relaxation was highest in vessels denuded of both PVAT and the endothelium. PVAT attenuated the relaxation response to thiopental, and this attenuation effect was Aldactone 25mg Tab reduced by both angiotensin II (Ang II) type 1 receptor antagonists CV-11974 (2-n-butyl-4-choloro-5-hydroxymethyl-1-[2'-(1H-tetrazol-5-yl)biphenyl-methyl]-imidazole) or losartan and the angiotensin-converting enzyme inhibitor enalaprilat. Thiopental at high concentration (3 × 10(-3) M) caused a contraction through an endothelin-dependent mechanism.

vasotec normal dosage 2017-01-07

EN blunted the rise in ischemic intracellular sodium, measured using MRS. With reperfusion, EN-treated hearts recovered 80% of their preischemic ventricular function, compared with negligible Cymbalta Migraine Dose recover, in controls. These beneficial effects of EN were blocked when the bradykinin receptor antagonist, HOE 140, was coadministered with EN. HOE 140 also blocked EN-mediated attenuation of ischemic intracellular acidosis.

vasotec 10 mg 2016-04-19

We have investigated the possible effects of contrasting ACE Paxil 60 Mg (I/D) genotypes on the responses to the ACE inhibitor enalaprilat in normotensive men.

vasotec generic names 2015-10-06

The angiotensin-converting enzyme (ACE) profile in urine of hypertensive patients and spontaneously hypertensive rats (SHR; 90- and 65-kDa N-domain ACEs) is different from that of healthy subjects and Wistar rats (190 and 65 kDa). In addition, four ACE isoforms were purified from mesangial cells (MC) of Wistar rats in the intracellular compartment (130 and 68 kDa) and as secreted forms (130 and 60 kDa). We decided to characterize ACE forms from SHR MC in culture. Analysis of the ACE gene showed that SHR MC are able to express ACE mRNA. The concentrated medium and cell homogenate were separately purified by gel filtration and then subjected to lisinopril-Sepharose chromatography. The molecular masses of purified enzymes, 90 kDa for ACEm1A and 65 kDa for ACEm2A (secreted enzymes) and 90 kDa Cymbalta Drug Usage for ACEInth1A and 65 kDa for ACEInth2A (intracellular), were different from those of Wistar MC. The purified enzymes are Cl- dependent, inhibited by enalaprilat and captopril, and able to hydrolyze AcSDKP. Immunofluorescence and cell fractionation followed by Western blotting showed predominant immunoreaction of the 9B9 antiserum for N-domain ACE in the nuclei. The N-domain ACE was localized in the glomerulus from Wistar rats and SHR. ANG II and ANG-(1-7) were localized in the cell cytoplasm and nuclei. The 90-kDa N-domain ACE, described recently as a possible genetic marker of hypertension, was found inside the cell nuclei of SHR MC colocalized with ANG II and ANG-(1-7). The presence of ANG II in the cell nuclei could suggest an important role for this peptide in the transcription of new genes.

vasotec drug contraindications 2015-03-01

Forty-six patients were randomly allocated to two different groups of treatment if their diastolic blood pressure remained above 90 mm Hg after one month of treatment with 20 mg enalapril mg once daily. In the first group (ENA), 23 patients were given higher daily dosages of enalapril (40 mg and, when necessary, 60 mg). The second group of 23 patients (HCTZ) was given 20 mg/day enalapril and hydrochlorothiazide (25 mg/day and, when necessary, 50 mg). Blood pressure was measured by an automatic device and by the physician with a standard sphygmomanometer. Blood pressure was significantly lower in the HCTZ group, according to both the automatic device (130 +/- 9/80 +/- 8 vs. 141 +/- 5/86 +/- 8 mm Hg, p less than 0.01/p less than 0.05) and the sphygmomanometer (134 +/- 10/89 +/- 6 vs. 149 +/- 16/94 +/- 5 mm Hg, p less than 0.001/p less than 0.01). Plasma renin activity, increased by enalapril at the 20 mg dosage, rose in the HCTZ group but not in the ENA group (22.4 +/- 22 vs. 10.2 +/- 11 pmol/ml/h, p less than 0.05). Plasma aldosterone increased significantly in the HCTZ group (0.44 +/- 0.22 vs. 0.30 +/- 0.17 pmol/ml, p less than 0.05) but did not change in the ENA group (0.31 +/- 0.11 vs. 0.30 +/- 0.17 pmol/ml, NS). In the ENA group, converting enzyme activity was not reinforced (5.7 +/- 8 vs. 6.6 +/- 6 mU/ml, NS) despite an increase in plasma enalaprilat levels (172.4 +/- 108 vs. 72.1 +/- 42 ng/ml, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)