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Minipress (Prazosin)

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Minipress is an effective strong preparation which is taken in treatment of hypertension diseases. Minipress is also helpful in treatment of male prostate enlargement symptoms, congestive heart failure, Raynaud's disease. Minipress acts as anti-hypertension remedy.

Other names for this medication:

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Lisinopril, Amlodipine, Norvasc, Benicar, Metoprolol, Hydrochlorothiazide, Avapro, Losartan


Also known as:  Prazosin.


Minipress is created by pharmacy specialists to combat hypertension disease. Target of Minipress is to control level of blood pressure.

Minipress acts as anti-hypertension remedy. Minipress operates by reducing blood pressure.

Minipress is also known as Prazosin, Prazopress, Vasoflex, Hypovase.

Minipress is alpha blocker.

Generic name of Minipress is Prazosin (oral).

Brand name of Minipress is Minipress.


You should take it by mouth with water.

It is better to take Minipress 2-3 times a day at the same time with meals or milk.

It is better to start the first Minipress dose when are going to bed.

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


If you overdose Minipress and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Minipress overdosage: feeling lightheaded, rash, weakness, troublesome breathing, pruritus, swelling.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

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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.


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

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

Be careful with Minipress if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Minipress if you have allergies to medicines, foods, or other substances.

Be careful with Minipress if you have liver or kidney disease, heart failure, low blood pressure, narcolepsy, prostate cancer.

Be careful with Minipress if you take muscle relaxants as carisoprodol; anti-anxiety drugs as diazepam; anti-seizure drugs as carbamazepine; tranquilizers; sleep medicines as sedatives; antihistamines as diphenhydramine; verapamil; psychiatric medicines as tricyclic antidepressants (amitriptyline), phenothiazines (chlorpromazine); sexual function problems drugs as vardenafil, sildenafil, tadalafil; narcotic pain relievers as codeine; beta blockers as metoprolol, propranolol, atenolol.

Avoid machine driving.

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

Avoid alcohol.

Minipress can be not safety for elderly people.

Try to be careful with sunbeams. Minipress makes skin sensitive to sunlight. Protect skin from the sun.

Do not stop taking Minipress suddenly.

minipress dosage forms

It was found that all these nine drugs significantly decreased BP in SAD rats. Six of these drugs (nifedipine, nitrendipine, amlodipine, clonidine, prazosin and atenolol) significantly decreased BPV in SAD rats, but the remaining three drugs did not. Clonidine and atenolol increased the heart period and the others did not. No drugs affected the heart period variability.

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Our objective was to evaluate immediate acute changes in myocardial function during the autonomic storm of brain death (BD). Wistar rats were divided into four groups (n = 8/group): controls without any treatment, β-blocker (Esmolol®, 10 mg/kg), calcium channel blocker (Diltiazem®, 10 mg/kg), or alpha-blocker (Prazosin®, 0.3 mg/kg). Treatments were administered intravenously 5 min before BD induction. Echocardiography (ATL-5000, 8 MHz) was performed to measure left ventricular (LV) dimensions and fractional shortening at baseline, during BD induction and 5 min and 15 min after BD. In controls, BD was immediately associated with an increase in wall thickness and a decrease in LV cavity dimension. This myocardial wall hypertrophy was completely prevented by β-blockers, but not with calcium- and alpha-blockers. Extensive myocardial interstitial edema was found in all groups, except in the β-blocker group. Myocardial wall hypertrophy was also prevented during a longer follow-up of 180 min after BD in β-blocker group as opposed to controls. In conclusion, BD is associated with an immediate and severe myocardial damage related to an important interstitial edema which is prevented by β-blockers.

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Enzymatic digestions were used to dissociate ICCs from mouse small intestine tissues. All experiments on ICCs were performed on within 12h after culture. A whole-cell patch-clamp configuration was used to record potentials (current clamp) from cultured ICCs. Intracellular Ca(2+) ([Ca(2+)]i) increase was studied in cultured ICCs using fura-2AM. All of the experiments were performed at 30-32°C.

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The efficacy and safety profiles were different among the alpha-1 blockers at standard doses. Tamsulosin appears to be safer than the others for aged patients or patients with hypertension who have impaired blood pressure regulation, while terazosin is significantly effective in improving symptomatic score when compared with the others examined. It is recommended that the alpha-1 blocking agent and its optimal dose are selected on the basis of the baseline characteristics of the patients with symptomatic BPH.

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The contractile responses of the longitudinal smooth muscle layer of the isolated guinea-pig ileum which were elicited by long-lasting (40 sec train duration) electrical field stimulation (0.8 msec, 20 V), applied at a frequency of either 5 or 30 Hz, comprised an initial phasic component followed by a secondary tonic contraction, were studied against the background of postsynaptically-acting receptor antagonists. Atropine and apamin reduced both components of the responses while prazosin produced no change. Propranolol induced a slight reduction, decreasing mainly the responses evoked by stimulation at a frequency of 5 Hz. The simultaneous application of cholinoceptor and adrenoceptor blockers revealed a non-cholinergic, non-adrenergic component of the responses. The putative prostaglandin antagonist, SC 19220 was found to reduce mainly the tonic component of the non-cholinergic, non-adrenergic contractions evoked by stimulation at both frequencies used. These results demonstrated that the two-component contractile responses of the guinea pig ileum to long-lasting electrical stimulation were due to the release of more than one neurotransmitter and/or spasmogenic substance. It is concluded that the initial phasic component was evoked by acetylcholine and by a non-cholinergic, non-adrenergic neurotransmitter, while the tonic component was maintained predominantly by prostaglandins released during stimulation.

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In the present study, Wistar rats, which received a streptozotocin injection to induce diabetes (STZ-diabetic rats), a model similar to insulin-dependent diabetes mellitus (IDDM) or type 1 diabetes mellitus, were used to investigate the effect of prostaglandin (PG) E2 on plasma glucose. Intravenous injection of PGE2 produced a dose-dependent lowering of plasma glucose level in fasting STZ-diabetic rats after 60 min. In addition to the blockade of this hypoglycemic effect by guanethidine (a noradrenergic nerve terminal-blocking agent), prazosin at a dose effective to block alpha1-adrenoceptors abolished the action of PGE2. An increase of plasma norepinephrine (NE) was also observed in STZ-diabetic rats receiving PGE2 injections. Participation of sympathetic stimulation by PGE2 may thus be speculated. Also, the plasma glucose-lowering effect of PGE2 was also blocked by pretreatment with naloxone or naloxonazine at doses sufficient to block opioid mu-receptor. Injection of PGE2 increased plasma beta-endorphin-like immunoreactivity (BER) in STZ-diabetic rats, and this action was abolished by prazosin. Bilateral adrenalectomy resulted in the loss of this PGE2 effect, and no increase was seen in plasma BER with PGE2 in STZ-diabetic rats. Therefore, beta-endorphin from the adrenal gland appears to be responsible for the lowering of plasma glucose in STZ-diabetic rats by PGE2 through an increase of NE release to activate alpha1-adrenoceptors.

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Intact chest preparation; adult mongrel cats.

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Alpha-adrenergic blockers are an established form of medical treatment for symptomatic benign prostatic hyperplasia (BPH). Several medications of the class are available, each with its own characteristics. The authors attempted to define the differences between the currently available medications (Terazosin, Doxazosin, Alfuzosin, and Tamsulosin), and to present an evidence-based recommendation for choosing the best treatment option. A literature search was conducted, using Medline queries and the references of review papers, in search of pertinent studies. These included controlled studies comparing the results of treatment with alpha blockers to placebo, or direct comparative studies of alpha blockers, and real life practice, community studies of each of the medications. A similar efficacy emerged from the reviewed articles, but with a different adverse events profile. A higher rate of vasodilatatory, cardiovascular side effects (dizziness, fatigue, and hypotension) was observed with terazosin and doxazosin, when compared with the uroselective alfuzosin and tamsulosin. Of the latter two, hypotension was more frequent with alfuzosin, while ejaculatory dysfunction was more frequent with tamsulosin. In conclusion, each of the four medications is a possible treatment option for BPH, but we believe alfuzosin and tamsulosin are the better choice. In light of an identical efficacy, these medications offer better tolerability, and ease of use of a once daily treatment without dose titration. The choice between the two should be tailored to the individual patient, with alfuzosin associated with hypotensive side effects, and tamsulosin causing ejaculatory dysfunction.

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The effect of four calcium antagonists (nifedipine, nitrendipine, nisoldipine, and verapamil) on hypoxia-induced changes in right ventricular parameters were examined in anesthetized closed-chest rats using an ultraminiature catheterization technique. The effect of the calcium antagonists was compared to the alpha-adrenoceptor blocker prazosin, the beta-adrenoceptor blocker propranolol, the angiotensin-converting enzyme (ACE) inhibitor captopril, and the vasodilator nitroglycerin. The animals were exposed to two successive 5-min hypoxic periods separated by a normoxic interval of 60 min, during which the animals received an intravenous (i.v.) infusion of the substances tested. Hypoxia caused a marked rise in right ventricular systolic pressure (RVSP) and a moderate increase in RVdP/dtmax. Heart rate (HR) was only slightly enhanced. The functional response to the second hypoxic period did not differ from the first one in NaCl-infused animals. All calcium antagonists reduced the hypoxic pressure increase in a dose-dependent manner and ultimately abolished it. Nisoldipine was the most effective substance, followed by nifedipine, nitrendipine, and verapamil. In contrast, prazosin and propranolol did not influence the hypoxic pressure response. Administration of captopril and nitroglycerin attenuated the increase in RVSP. Thus, as compared with the other substances tested, calcium antagonists were the most effective drugs that antagonized the hypoxia-induced increase in RVSP.

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Pre-eclampsia is still a very prevalent disease with critical hemodynamic changes. This study was evaluated the major anti-hypertensive schemes used at the Materno Perinatal Hospital "Monica Pretelini" (HMPMP) hospitalized at the Obstetric Intensive Care Unit (OICU) for at least seven days. In other group of patients we compared hemodynamic monitoring with Swan-Ganz catheter versus transthoracic electrical bioimpedance (TEB) and gasometric formulas. Statistical analysis was done using the Statistical Package for Social Science (SPSS) software, version 17. Amlodipine + temisartan + prazocin was the preferred anti-hypertensive drug combination used in our intensive care unit. Sodium nitroprusside is required in 25% of patients until reaching control. There was no statistically significant difference in cardiac output calculated with gasometric formulas compared to thermodilution with Swan-Ganz catheter. Calcium antagonists + angiotensin II receptor blocker (ARB) + α-blockers offer the best option to control hypertension in puerperal women that followed pre-eclampsia, but oral and IV drugs to control hypertension is required in 20% of cases, in a Mexican Intensive Care Unit specialized in obstetrical patients. Hemodynamic monitoring with gasometric formulas is still usefull in this set of patients, without discarding TEB with a correction factor due to the accumulated extravascular water in these patients.

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The cardiovascular effects of the new histamine H2 receptor agonist amthamine were studied in the anaesthetized rat, with particular reference to a possible interaction with the adrenergic system. Amthamine (0.03-3 mumol/kg i.v.) caused vasodepressor responses which were antagonized by famotidine (3 mumol/kg i.v.). At higher doses (30-100 mumol/kg i.v.), amthamine induced a modest increase in the mean arterial pressure, which was significantly enhanced by the blockade of H2 receptors and significantly reduced by the alpha 2 adrenoceptor antagonist yohimbine (1 mumol/kg i.v.). The vasopressor response to amthamine was not modified in rats pre-treated with reserpine or 6-hydroxydopamine, and was only minimally modified in adrenalectomized animals, thus suggesting a predominant interaction with postjunctional alpha 2 adrenoceptors in the vascular muscle. The H2 receptor agonist dimaprit (0.3-100 mumol/kg i.v.) caused a reduction in arterial pressure, which was antagonized by famotidine, no pressor response being unmasked. Dimaprit (0.1-30 mumol/kg i.v.) did not modify heart rate but caused a modest bradycardia at 100 mumol/kg i.v. Amthamine (1-100 mumol/kg i.v.) induced a dose-dependent tachycardia, which was only partially (approximately 20%) reduced by famotidine and was totally blocked by propranolol (0.3 mg/kg i.v.). This effect was significantly reduced in rats pre-treated with reserpine or 6-hydroxydopamine and was further reduced by cocaine, thus suggesting a tyramine-like action of amthamine. In conclusion, these data demonstrate that the H2 receptor agonist amthamine can also interact with the adrenergic system when used at doses higher than those necessary to activate H2 receptors. Whereas the increase in blood pressure induced by amthamine seems to be mainly mediated by a direct activation of postjunctional alpha 2 adrenoceptors, the increase in heart rate is predominantly due to neuronal release of catecholamines. These effects should be considered when using amthamine in cardiovascular or other studies when high doses are employed.

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A total of 52 pigs were anesthetized. A double lumen 6Fr catheter was inserted through each renal pelvis and into the ureter, allowing perfusion of saline or drug solution into the renal pelvis and the recording of contractions from the mid portion of the ureter.

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This study confirmed prostate hyperplasia in the SHR model. Doxazosin exposure did not reduce the volume of glandular epithelium and contributed to protecting against caspase-induced apoptosis. The SHR model may be not a valid option to study doxazosin-induced apoptosis in BPH.

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Alpha-1 and alpha-2 adrenoceptor-mediated vasoconstriction was studied in the in situ, autoperfused pulmonary circulation of the open-chest anesthetized dog under conditions of normal and elevated pulmonary vascular tone. Under conditions of normal pulmonary vascular tone (10 +/- 1 mm Hg), methoxamine, a selective alpha-1 adrenoceptor agonist, and B-HT 933, a selective alpha-2 adrenoceptor agonist, elicited maximal increases in lobar perfusion pressure of 5 and 2 mm Hg above resting pulmonary tone, respectively. When pulmonary vascular tone was elevated progressively with the thromboxane mimetic, U-46619, serotonin or PGF2 alpha, alpha-1 adrenoceptor-mediated pulmonary vasoconstrictor responses to methoxamine were unaffected, whereas alpha-2 adrenoceptor-mediated pulmonary pressor responses to B-HT 933 were enhanced. Overall the response to B-HT 933 was enhanced 4-fold when pulmonary perfusion pressure was elevated to 19.8 +/- 0.8 mm Hg with U-46619 and almost 5-fold when elevated to 27.0 +/- 1.2 mm Hg. Pulmonary vasoconstrictor responses to angiotensin II were unaffected by elevated pulmonary vascular tone. Enhanced responsiveness of B-HT 933 to elevated pulmonary vascular tone was antagonized by the selective alpha-2 adrenoceptor antagonist, rauwolscine (100 micrograms/kg i.v.), and unaffected by the selective alpha-1 adrenoceptor antagonist, prazosin (100 micrograms/kg i.v.). When canine intralobar pulmonary veins were studied in vitro they contracted to B-HT 933 whereas intralobar pulmonary arteries did not respond. These data indicate that alpha-2 adrenoceptor responsiveness is enhanced markedly and selectively under conditions in which pulmonary vascular tone is elevated.

minipress medication information

In dogs anesthetized with pentobarbital sodium (30 mg/kg iv), infusions of phenylephrine (PE; 1-3 iv for 30 min and longer) caused sustained elevations in blood pressure and suppressed depressor responses to acetylcholine (ACh; 1 microgram/kg iv) in a dose- and time-dependent manner. The dose-response curve for ACh (0.01-100 micrograms/kg iv)-induced depressor responses was shifted to the right by approximately 80-fold after an intravenous infusion of PE (3 for 120 min. Similar suppression was observed when infusions of methoxamine (5 iv), norepinephrine (3 iv under blockade of beta-adrenoceptors), or angiotensin II (0.3 iv) were carried out. However, in dogs treated with prazosin (1 mg/kg iv) or hydralazine (1 mg/kg iv) to prevent elevations in blood pressure over the baseline level, PE (3 iv) failed to attenuate depressor responses to ACh. The suppression observed after PE infusion was specific to ACh-induced depressor responses; i.e., no suppression was observed on the depressor responses to other drugs, such as histamine, sodium nitroprusside, carbachol, and methacholine. Furthermore, neostigmine (bolus injection of 30 microgram/kg iv followed by an infusion of 15 iv) greatly diminished the suppressive effect of PE. Except for a slight increase in acetylcholinesterase (AChE) activity in renal arterial segments, activities of both AChE and butyryl-cholinesterase in plasma, erythrocytes, and pulmonary and renal arterial segments were unchanged after PE infusion. These results suggest that prolonged elevation in blood pressure and/or vasoconstriction selectively attenuates depressor responses to ACh through accelerated degradation of this material.

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To study the effect of phentolamine on L-type calcium currents (ICa) and ATP-sensitive K+ currents (IK,ATP) in ventricular myocytes.

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The effects of cocaine were studied in an identifiable RP4 neuron of the African snail, Achatina fulica Ferussac, using the two-electrode voltage-clamp method. The RP4 neuron generated spontaneous action potentials and bath application of cocaine (0.3-1 mM) reversibly elicited action potential bursts of the central RP4 neuron in a concentration-dependent manner. The action potential bursts were not blocked when neurons were immersed in high-Mg(2+)solution, Ca(2+)-free solution, nor after continuous perfusion with atropine, d-tubocurarine, propranolol, prazosin, haloperidol, or sulpiride. Similarly, the action potential bursts were not abolished by pretreatment with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride, (9S,10S,12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid hexyl ester or anisomycin. Injection of hyperpolarizing current at an intensity of greater than 2 nA effectively suppressed the cocaine-elicited action potential bursts and no postsynaptic potentials were observed under these conditions. These results suggest that the generation of action potential bursts elicited by cocaine was not due to (1) the synaptic effects of neurotransmitters, (2) the cholinergic, adrenergic or dopaminergic receptors of the excitable membrane, or (3) the cAMP second messengers and new protein synthesis of the RP4 neuron. Notably, the induction of action potential bursts was blocked by pretreatment with 1-[6-[((17beta)-3-methoxyestra-1,3,5[10]-trien-17-yl)amino]hexyl]-1H-pyrrole-2,5-dione. Voltage-clamp studies conducted on the RP4 neuron revealed that cocaine at 0.3 mM decreased (1) the Ca(2+) current, (2) the delayed rectifying K(+) current, (3) the fast-inactivating K(+) current and (4) the Ca(2+)-activated K(+) current, but had no remarkable effects on the Na(+) current. Perfusion with Ca(2+)-free solution, which may abolish the Ca(2+) current and Ca(2+)-activated K(+) current, did not cause any bursts of action potentials in control RP4 neurons. Application of 4-aminopyridine, an inhibitor of fast-inactivating K(+) current, and paxilline, an inhibitor of Ca(2+)-activated K(+) current, failed to elicit action potential bursts, whereas tetraethylammonium chloride, a blocker of Ca(2+)-activated K(+) current and delayed rectifying K(+) current, and tacrine, an inhibitor of delayed rectifying K(+) current, successfully elicited action potential bursts. Further, while 1-[6-[((17beta)-3-methoxyestra-1,3,5[10]-trien-17-yl)amino]hexyl]-1H-pyrrole-2,5-dione did not affect the delayed rectifying K(+) current of the RP4 neuron, 1-[6-[((17beta)-3-methoxyestra-1,3,5[10]-trien-17-yl)amino]hexyl]-1H-pyrrole-2,5-dione decreased the inhibitory effect of cocaine on the delayed rectifying K(+) current. It is concluded that cocaine elicits action potential bursts in the central snail RP4 neuron and that the effect is closely related to the inhibitory effects on the delayed rectifying K(+) current.

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A pharmacological approach was employed in order to visualize a Ca2(+)-dependent component of the extracellularly recorded nerve terminal impulse in the secretory regions of the sympathetic postganglionic nerves in the rat tail artery. Application of potassium-channel-blocking agents within the recording electrode caused the nerve terminal impulse to acquire a delayed negative deflection, which we have termed the late negative component (LNC) of the nerve terminal impulse. The time course and the latency of the LNC differed from that of the postjunctional transmitter-induced excitatory junction current, and the LNC persisted when the excitatory junction current was blocked by adenosine [alpha,beta-methylene]triphosphate, and was resistant to the alpha 1-antagonist prazosin and the alpha 2-antagonist yohimbine. Probably, therefore, the LNC was exclusively prejunctional in origin. For the following reasons it seems likely that the LNC, at least in part, was caused by influx of Ca2+ into the secretory regions of these nerves: (a) the LNC occurred only when potassium-blocking agents were present within the recording electrode; (b) the LNC amplitude increased with the Ca2+ concentration inside the recording electrode and was reduced by the removal of Ca2+; (c) the LNC was enhanced by replacing Ca2+ in the medium inside the recording electrode with Ba2+; (d) the LNC was depressed by the inorganic Ca2(+)-channel blocker cadmium or the Ca2(+)-channel-blocking peptide omega-conotoxin added within the recording electrode only, or by addition of cadmium or cobalt (but not the organic Ca2(+)-channel blocker nifedipine) inside and outside the recording electrode.(ABSTRACT TRUNCATED AT 250 WORDS)

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The rats were divided into 6 groups: Control, DOCA, L-NAME, L-NAME+DOCA, L-NAME+ prazosin, and L-NAME+DOCA+prazosin. Tail systolic BP was measured twice a week. After a 6-week evolution, mean arterial pressure (MAP) was measured, along with selected metabolic, morphological and renal variables.

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The gigantocellular depressor area (GiDA) is a functionally defined subdivision of the medullary gigantocellular reticular formation where vasodepressor responses are evoked by glutamate nanoinjections. The GiDA also contains reticulospinal neurons that contain the alpha2A-adrenergic receptor (alpha2A-AR). In the present study, we sought to determine whether nanoinjections of the alpha2-AR agonist clonidine into the GiDA evoke cardiovascular responses and whether these responses can be attributed to the alpha2-AR. We found that nanoinjections of clonidine into the GiDA evoke dose-dependent decreases in arterial pressure and heart rate. These responses were equivalent in magnitude to responses produced by clonidine nanoinjections into the sympathoexcitatory region of the rostral ventrolateral medulla. Furthermore, the vasodepressor and bradycardic responses produced by clonidine injections into the GiDA were blocked in a dose-dependent fashion by the highly selective alpha2-AR antagonist 2-methoxyidazoxan, but not by prazosin, which is an antagonist at both the alpha1-AR and the 2B subtype of the alpha-AR. The antagonism by 2-methoxyidazoxan was site specific because injections of the antagonist into the rostral ventrolateral medulla failed to block the responses evoked by clonidine injections into the GiDA. These findings support the notion that clonidine produces sympathoinhibition through multiple sites within the medullary reticular formation, which is consistent with the wide distribution of the alpha2A-AR in reticulospinal neurons. These data also suggest that clonidine may have multiple mechanisms of action because it evokes a cardiovascular depressive response from regions containing neurons that have been determined to be both sympathoinhibitory and sympathoexcitatory.

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These findings indicate that: (i) radioligand binding can be applied in intact arterial segments to quantify and characterize alpha 1-AR; (ii) although differences seem to exist between rat strains, alpha 1B-AR and alpha 1D-AR predominate in rat thoracic aorta and alpha 1A-AR and alpha 1B-AR in mesenteric small arteries; and (iii) alpha 1-AR density is not reduced in the poorly innervated aorta and the densely innervated mesenteric small arteries of rats with heart failure due to myocardial infarction.

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The alpha(1)-adrenergic mediated contraction, Ca(2+) signaling and the subcellular receptor distribution were evaluated using the Fluo-4, BODIPY-FL prazosin and subtype-specific antibodies.

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minipress medication information 2015-09-10

1. Total inositol phosphate formation was measured in labelled femoral and iliac arteries and veins of 14 week-old spontaneously hypertensive rats (SHR) and age-matched Wistar Kyoto (WKY) controls, either unstimulated or in the presence of noradrenaline. 2. Basal levels of [3H]-inositol phosphates and [3H]-phosphatidylinositol were significantly enhanced in SHR femoral artery, but not in the other 3 vessels, compared with WKY. 3. Noradrenaline stimulated phosphoinositide hydrolysis in all four vessels of SHR and WKY. Pretreatment with prazosin (10(-7)-10(-6) M) but not with yohimbine (10(-7) M), inhibited the noradrenaline-induced inositol phosphate formation indicating an alpha 1-adrenoceptor buy minipress -mediated response. 4. In the femoral artery of SHR compared to WKY, [3H]-inositol phosphate accumulation induced by noradrenaline (10(-7)-10(-5) M) was significantly reduced when expressed relative to basal values although the response to higher concentrations (10(-4)-10(-3) M) was not altered. In contrast, a significant reduction of inositol phosphates was seen only with 10(-7) M noradrenaline when absolute values were compared. In the other three vessels, no difference in noradrenaline-induced [3H]-inositol phosphate formation was observed between strains. 5. These data suggest that phosphoinositide hydrolysis-mediated by alpha 1-adrenoceptors may be reduced in some but not all blood vessels of adult SHR.

minipress xl tablets 2016-04-08

1. The effects of the alpha-adrenoreceptor antagonists, prazosin and yohimbine, have been examined on buy minipress the isometric contraction of the rabbit pulmonary artery produced by alpha 1-adrenoreceptor agonists. Cocaine, corticosterone and propranolol were present throughout and either a single or two concentration-response curve method was used. 2. Prazosin and yohimbine competitively antagonized the responses to agonists but did not reveal differences between agonists. 3. Using the single concentration-response curve method, prazosin had pA2 values of 9.06 against clonidine and 8.76 against methoxamine. 4. Using the two concentration-response curve method the absolute pA2 values of prazosin (8.65 against phenylephrine, 8.78 against clonidine) and yohimbine (5.73 against phenylephrine, 5.72 against clonidine), as well as the relative potencies of the two antagonists (prazosin approximately 1000 times more potent than yohimbine), suggest that both agonists act on alpha 1-adrenoreceptors. 5. There is no evidence from this study to support the suggestion that the rabbit pulmonary artery contains two subtypes of alpha 1-adrenoreceptor.

minipress 6 mg 2015-09-11

These studies examined the effects of the alpha-adrenergic agonist clonidine on spontaneous and synaptically evoked activity in the solitary tract nucleus in superfused rat brain slices. In one group of neurons which showed no spontaneous spike activity (n = 27), clonidine superfusion induced a dose-dependent increase of postsynaptic responsiveness buy minipress to input from the ipsilateral solitary tract. In another group of neurons which were spontaneously active but unresponsive to tract input (n = 20), clonidine induced a dose-dependent depression of spontaneous discharge. A third group of neurons which were both spontaneously active and responsive to tract input (n = 11) showed primarily a depression of both activities. The neuronal responses to clonidine in all 3 groups were selectively blocked by the alpha 2-adrenoceptor antagonist yohimbine but not by the alpha 1-antagonist prazosin. These results provide insight into the possible actions of endogenous adrenergic systems in the synaptic processing of afferent sensory information within the solitary tract nucleus.

minipress and alcohol 2016-01-25

Forty-one men over the age of 50 years with an American Urological Association (AUA) symptom score greater than 8, postvoid residual urine volume (PVR) less than 300 mL, and no clinical or biochemical evidence of prostate cancer were treated with terazosin independent of the baseline PFR. The effect of terazosin on the AUA symptom score and PFR were compared for subjects with a PFR of 15 mL/s or less (group I) and those with a PFR greater than 15 mL/s (group II). buy minipress

minipress tablets dose 2016-07-14

The effect of normoxia, hypoxia and hypercapnia on the extracellular pH, partial pressure carbon dioxide (pCO2), partial pressure oxygen (pO2) and HCO3- levels after noradrenaline treatment of Rana balcanica erythrocytes, was investigated buy minipress . Noradrenaline caused a significant reduction of the extracellular pH which may have been due to the activation of red blood cell Na+/H+ exchange. Significant falls in the partial extracellular pressure of CO2 and O2 were evident. The initial reduction in extracellular pCO2 and pO2 was followed by a rise reflecting the desensitization of the Na+/H+ exchange after 15 min of hormone stimulation. Both hypercapnia and hypoxia increased the magnitude of these changes in relation to normoxia, although the greatest changes were observed under hypercapnic conditions. The involvement of alpha 1 receptors in regulating the concentration of respiratory gases after catecholamine stimulation was demonstrated. It is suggested that these responses increased the effectiveness of gas transfer over the respiratory surfaces.

minipress dosage forms 2017-04-07

The objective of the present study was to explore the effect of carvedilol treatment on metabolic parameters in patients with metabolic syndrome. A total of 77 patients > or = 20 years of age (59 females, 18 males, mean age, 52.3 +/- 10.3) with stage 1 hypertension who fulfilled at least 3 of the metabolic syndrome criteria proposed by NCEP-ATP III were included in this prospective, randomized, controlled study. Patients were randomly assigned to receive daily treatment with carvedilol (n = 27, 12.5 mg/day orally for the first 2 days and 25 mg/day thereafter), atenolol (n = 26, 50 mg/day orally), or doxazosin (n = 24, 2 mg/day orally) for 90 days. Doses were doubled at the end of the 3rd week in patients whose blood pressure was inadequately controlled and amlodipine 10 mg was added to the treatment if the target blood pressure was still not reached at the end of week 6. The biochemical parameters and insulin sensitivity based on the HOMA-IR model were evaluated at baseline and at the end of treatment. Similar reductions in systolic and diastolic blood pressure were observed in all groups (P > 0.05). A significant decrease in HDL cholesterol levels occurred in the doxazosin and atenolol groups compared to the buy minipress carvedilol group (percent change: -5.6 +/- 13.5 and -8 +/- 9.8 versus -0.1 +/- 12.2, respectively; P < 0.05) and a significant increase in apolipoprotein A1 level was observed in the carvedilol group compared to the doxazosin and atenolol groups (percent change: + 4.3 +/- 9.6 versus - 0.5 +/- 10.6 and -2.3 +/- 6.6, respectively; P < 0.05). There were no significant differences among the groups with respect to other parameters. It is concluded antihypertensive treatment with carvedilol in patients with metabolic syndrome effectively reduces blood pressure without adversely affecting metabolic parameters.

minipress drug information 2016-10-06

Tizanidine [5-chloro-4-(2-imidazolin-2-yl-amino)-2,1,3-benzothiadiazole] is able to increase the pain threshold in the tail-flick test in mice. The effect of tizanidine was investigated after treatment of mice with drugs influencing central monoaminergic and GABAergic mechanisms. A drug that inhibits the synthesis and storage of monoamines and drugs that cause specific lesions of monoaminergic neurons had no consistent effect on the antinociceptive action of tizanidine. The action of tizanidine was antagonized by the alpha 2-adrenoreceptor antagonist, yohimbine, but not by the alpha 1 antagonist prazosin, nor by dopamine, serotonin buy minipress and GABA receptor antagonists. These results indicate that the antinociceptive action induced by tizanidine may be mediated by alpha 2-adrenoreceptors.

minipress xl dosage 2017-09-30

The main biological role of angiotensin II type 2 receptor (AT2) has not been established. We made use of targeted disruption of the mouse AT2 gene to examine the role of the AT2 receptor in the central nervous system (CNS). AT2- buy minipress deficient mice displayed anxiety-like behavior compared with wild-type mice. However, AT2-deficient mice showed no depressant-like activity and no change in hexobarbital-induced sleeping time as compared with findings in wild-type mice. Both noradrenergic and corticotropin-releasing factor (CRF) neuronal systems appear to be involved in this anxiety-like behavior. Diazepam, captopril (angiotensin I converting enzyme inhibitor), prazosin (alpha1 antagonist) reversed the anxiety-like behavior in these AT2-deficient mice, whereas yohimbine (alpha2 antagonist), phenylephrine (alpha1 agonist), clonidine (alpha2 agonist), isoproterenol (beta1/beta2 agonist), propranolol (beta1/beta2 antagonist) and alpha-helical CRF9-41 (CRF receptor antagonist) has no apparent effects on anxiety-like behavior in AT2-deficient mice. In addition, concentrations of plasma adrenocorticotropic hormone (ACTH) and corticosterone in AT2-deficient mice did not differ from these in wild-type mice, hence, there are probably no endocrine abnormalities involving the hypothalamic-pituitary-adrenal axis (HPA). The amygdala appears to play an important role in many of the responses to fear and anxiety. The number of [3H]prazosin but not [125I]CRF binding sites in the amygdala was significantly reduced in AT2-deficient mice. These findings indicate that the noradrenergic system is involved in mediating the anxiety-like behavior in AT2-deficient mice.

minipress drug class 2015-04-13

Acute generalized exanthematous pustulosis (AGEP) is a rare cutaneous eruption mainly provoked by drugs. A case of AGEP in a 74-year-old male that was attributed to the ingestion of terazosin hydrochloride is presented. This is the first reported case of this association in medical literature. The history, clinical presentation, and pathogenesis of AGEP are buy minipress discussed.

tab minipress dosage 2015-05-15

The autonomic innervation of the seminal vesicle from 8 and 16 week streptozotocin-induced diabetic rats and age-matched controls was studied by pharmacological, histochemical and immunohistochemical methods. Contractions in response to electrical field stimulation, which were abolished using prazosin (2 microM) or tetrodotoxin (one to 1.6 microM), and to noradrenaline were significantly increased in both eight and 16 week diabetic animals. The contractile response to acetylcholine was significantly increased in the 16 week diabetic rats only, when compared with controls. Although these responses were significantly increased, no difference was found in ED50 and buy minipress EF50 values between control and diabetic rats. Vasoactive intestinal polypeptide (0.3 microM) had no effect on resting tension or nerve-mediated responses. In seminal vesicles from control animals, both vasoactive intestinal polypeptide-immunoreactive and acetylcholinesterase-containing nerves were localised around the folds of the columnar epithelium of secretory cells, in contrast to neuropeptide Y-immunoreactive and catecholamine-containing nerves which were found in the smooth muscle layers. In seminal vesicles from both eight and 16 week diabetic animals no difference was seen in distribution or density of acetylcholinesterase-containing nerves; there was an increase in density and fluorescence intensity of vasoactive intestinal polypeptide- and neuropeptide Y-immunoreactive nerves and a decrease in catecholamine-containing nerves compared with controls. The results are discussed in relation to autonomic neuropathy in diabetes.

minipress overdose death 2016-04-01

Flupirtine is a new non-opioid, non-addicting centrally acting analgesic. In animals, antinociceptive activity of flupirtine was attenuated after reserpine buy minipress pretreatment or in the presence of alpha-adrenergic antagonists suggesting the possible involvement of the noradrenergic system in its analgesic mode of action. Additionally, flupirtine possesses skeletal muscle relaxing activity in rats.

minipress medication 2017-05-26

alpha2-Adrenergic receptors (alpha2ARs) are essential components of the neural circuitry regulating cardiovascular function. The role of specific alpha2AR subtypes (alpha2a, alpha2b, and alpha2c) was characterized with hemodynamic measurements obtained from strains buy minipress of genetically engineered mice deficient in either alpha2b or alpha2c receptors. Stimulation of alpha2b receptors in vascular smooth muscle produced hypertension and counteracted the clinically beneficial hypotensive effect of stimulating alpha2a receptors in the central nervous system. There were no hemodynamic effects produced by disruption of the alpha2c subtype. These results provide evidence for the clinical efficacy of more subtype-selective alpha2AR drugs.

minipress 1mg tablet 2016-04-24

The Brief Psychiatric Rating Scale (BPRS) and Neuropsychiatric Inventory (NPI) at Weeks 1, 2, 4, 6, and 8. The Clinical Global Impression buy minipress of Change (CGIC) at Week 8.

minipress medicine 2015-10-05

1. It is well known that alpha 1A-adrenoceptors have binding sites for imidazolic and for phenylethylaminic drugs. A study was made relating alpha 1A-adrenoceptor involvement in cardiovascular responses to intracerebroventricular (ICV) injection of BHT-920, an imidazoliclike drug, and phenylephrine, a phenylethylaminic drug, in conscious sham-operated and sinoaortically-denervated rats. 2. In sham-operated rats, cardiovascular responses to BHT-920 (30 micrograms, ICV) were increase of blood pressure and bradycardia but in sinoaortically denervated rats, after the pressor response, a decrease of blood pressure was also seen. The pressor and bradycardic responses to agonist were greater in sinoaortically denervated rats than in sham-operated rats. Phenylephrine (90 micrograms, ICV) showed a biphasic effect on blood pressure: an increase followed by a decrease, and bradycardia. The cardiovascular responses to phenylephrine in sinoaortic-denervated rats were greater than in sham-operated rats. 3. In sinoaortically denervated and sham-operated rats subchronically treated with the alpha 1-adrenoceptor antagonist prazosin (0.5 mg kg-1, intraperitoneally twice daily, for 6 days), an increase of cardiovascular responses to ICV administration of BHT-920 and phenylephrine was seen. 4. Baroreceptor deafferentation by sinoaortic denervation enhances the cardiovascular responses to BHT-920 and phenylephrine. The effects of BHT-920 buy minipress could be mediated by brain alpha 1A adrenoceptors because this agonist has an imidazoliclike structure; phenylephrine could also be activating central alpha 1A-adrenoceptors. The enhanced cardiovascular responses after prazosin treatment could also be due to a supersensitivity of brain alpha 1A-adrenoceptors.

minipress 4 mg 2015-09-07

1. Age-related changes in the reactivity of postsynaptic alpha-adrenoceptors of isolated portions (epididymal and prostatic) and in whole vas deferens have been studied using 4, 12 and 20 month-old rats. 2. The pD2 values for adrenaline-induced contractions were reduced in the epididymal portion and whole vas deferens of middle-aged and old animals, but not in the prostatic portion. No age related change to phenylephrine or clonidine sensitivity was observed. 3. pA2 values of prazosin and yohimbine were not changed by aging in any preparation. Phentolamine pA2 values were reduced in the Periactin 4mg Dose epididymal portion and in the whole vas deferens when adrenaline, but not when phenylephrine concentration-response curves were displaced by the antagonist. The mean pA2 value of yohimbine (6.78) indicates that this antagonist blocks alpha(1)-adrenoceptors in the rat vas deferens. 4. The data presented here suggest that age-related decreases in the sensitivity to adrenaline and phentolamine (when measured by displacing adrenaline concentration-effect curves) in the whole vas deferens are probably due to a variation in the proportion of alpha(1)-adrenoceptor subtypes in the epididymal portion of the rat vas deferens.

minipress 2 mg 2016-05-21

Effects of 5-[2-[(3-tert-butylamino-2-hydroxypropylthio)-4-thiazolyl]-2- thiophenecarboxamide hydrochloride (arotinolol, S-596) on hemodynamic and adrenergically induced renin release and renal vasoconstriction were investigated in pentobarbital anesthetized dogs. Arotinolol (1 mg/kg i.v.) decreased systemic blood pressure (SBP), heart rate (HR) and renin secretion rate without change in renal blood flow. Degree of hypotension induced by arotinolol and basal plasma renin activity prior to the injection of the drug showed significant correlation. Arotinolol (20 micrograms/min) produced significant suppression of renal nerve stimulation (RNS Minipress Xl Tablets )-induced renin release and attenuated an increase in renal vascular resistance during RNS at 3 Hz. The same extent of inhibition in the renin secretion response to RNS was also obtained during the infusion of dl-propranolol (100 micrograms/min). The renal vasoconstriction induced by RNS and norepinephrine (NE) was inhibited dose-dependently during the infusion of arotinolol (10, 30 and 100 micrograms/min), phentolamine (3, 10 and 30 micrograms/min) or prazosin (1, 3 and 10 micrograms/min). Arotinolol and prazosin exerted a greater inhibitory effect on RNS- than NE-induced vasoconstriction, and the opposite was true of phentolamine. Arotinolol dose-dependently decreased SBP and HR in a dose range of 0.01 to 3.0 mg/kg. The greater reduction in HR was observed with arotinolol at a lower dose range (0.01 to 0.1 mg/kg) than with propranolol. Arotinolol produced larger reduction of SBP, and less increase in carotid, vertebral, renal and external iliac vascular resistances than propranolol. These results suggest that arotinolol posesses a- and beta-adrenoceptor blocking properties, which effectively contribute to the suppression of the adrenergically induced renin release and renal vasoconstriction, and to the hypotensive effect.

minipress drug 2017-09-20

A rat gene and brain cDNA (pA2d) encoding the homologue of the human alpha-C4 adrenergic receptor subtype were isolated and characterized. RNA blots indicate that this gene is expressed in brain, heart and kidney but not in lung, liver or pancreas. Yohimbine, WB-4101 and prasozin all exhibited high affinity for this receptor in binding studies. Clonidine was more potent and efficacious than norepinephrine in inhibiting forskolin-stimulated cAMP production in CHO cells expressing pA2d. Together, these data suggest that the alpha 2-C4 gene product defines a previously undescribed pharmacological Biaxin Xl Dosing subtype of alpha 2-adrenergic receptor.

minipress generic name 2015-08-28

Hydralazine has been used widely to reduce tumor blood flow and thereby to induce hypoxia and to reduce extracellular pH (pHe) in tumors. Here we have investigated and compared the effects of the vasodilating drugs hydralazine, captopril, nifedipine, prazosin, sodium nitroprusside, and labetalol to reduce pHe in EMT-6 and KHT tumors of mice and to cause antitumor effects. After a single injection, captopril Nexium Maximum Dosage was most effective in reducing pHe in EMT-6 tumors with a decrease in mean pHe from 6.93 to 6.67 at 2 h after injection, while nifedipine was most effective for KHT tumors with a decrease in mean pHe from 6.96 to 6.75 at 1 h after injection. During 72 h of chronic administration into mice bearing tumors, nifedipine was ineffective in reducing pHe, but both captopril and hydralazine caused a small but significant reduction of pHe. Captopril caused significant delay in growth of the tumors, but had only a small effect on clonogenic cell survival. Captopril appears to be the most effective vasodilating drug to enhance tumor acidity.

minipress capsules 2015-07-31

In view of existing reports documenting that "in vitro" norepinephrine (NE) contracts ring-shaped rat aortic preparations, whereas it relaxes arterial Zithromax Loading Dose strips mounted in longitudinal fashion within an organ bath: it was decided to explore possible reasons which may account for such disparate actions of the same agonist on the same tissue. Isolated rings (circular preparations) obtained from rat thoracic aortae responded to increasing concentrations of NE with dose-dependent tonic enhancement, not significantly affected by the presence of indomethacin (10(-6)M); whereas, preincubation with phentolamine (10(-6)M), yohimbine (10(-7)M) or prazosin (10(-8)M), shifted significantly to the right points of the positive inotropic dose-response curve for NE. On the contrary longitudinally mounted preparations of rat aortic stips, reacted to increasing concentrations of NE with dose-dependent relaxation, an effect not modified by the presence of a beta-adrenoreceptor blocker, namely propranolol (10(-6)M). However, in presence of alpha-adrenoreceptor blockers, such as phentolamine (10(-6)M), yohimbine (10(-7)M) or prazosin (10(-8)M), the negative inotropic dose-response curve for NE was shifted to the right whereas in the presence of indomethacin (10(-6)M) or of tranylcypromine (2.5 x 10(-4)M), the NE-induced relaxation was either abolished or significantly displaced to the right, respectively. In another series of experiments the generation of labelled 6-keto-prostaglandin F1 alpha (the most important non-enzymatic metabolite of prostacyclin) by chopped rat aortae incubated for one hour with (1-14C)-arachidonic acid, was explored and found to be significantly enhanced by the delivery of NE (3 x 10(-6)M). The present evidence suggests that NE acting on alpha-adrenoreceptors, induces in longitudinal and in chopped arterial preparations, but not in aortic rings, an inhibitory relaxing factor, presumably produced by the endothelium. This factor is probably prostacyclin for the relaxing effects of the agonist were negatively influenced by indomethacin and by tranylcypromine, two known antagonists of PGI2 formation. In vascular rings (circular arterial preparations) the tonic stimulatory action of NE (not affected by preincubation with indomethacin) was the only evident inotropic effect of the agonist presumably because the extensive handling of the tissue as well as the anchoring procedure followed to mount arterial preparations within the bath for contractile recordings, may produce de-endothelization.(ABSTRACT TRUNCATED AT 400 WORDS)

minipress xl dose 2017-01-05

The effect of oxaprotiline (OXA) enantiomers--of which (+)-OXA inhibits noradrenaline (NA) uptake, whereas (-)-OXA does not--on the secretion of adrenocorticotropin hormone (ACTH) and corticosterone was studied in rats. Both enantiomers dose-dependently and with a similar potency increased the plasma level of ACTH and corticosterone, the effect of (-)-OXA on corticosterone being of a longer duration. The stimulation of ACTH secretion and the inability of (+)- and (-)-OXA to increase the plasma corticosterone concentration in animals pretreated with dexamethasone indicate that secretion of the latter hormone results from the action of the enantiomers at a level superior to the adrenal cortex, i.e. the hypothalamus/pituitary. The corticosterone response to (+)- or (-)-OXA was not modified in rats with a selective lesion of NA nerve endings induced by the neurotoxin DSP-4, nor was it affected by the selective alpha 1-antagonist prazosin, the selective alpha 2-antagonist yohimbine, the mixed alpha 1/alpha 2-antagonist phentolamine, the selective dopamine (D2) receptor antagonist sulpiride Aciphex Generic Complaints and the non-selective 5-hydroxytryptamine (5-HT) receptor antagonist metergoline. These results indicate that neither the NA system nor D2 and 5-HT receptors are involved in the hormonal response to the OXA enantiomers. Although the (+)- and (-)-OXA-induced stimulation of corticosterone secretion was not antagonized by diazepam, ipsapirone, naloxone, or propranolol, it cannot be excluded that both these enantiomers act as non-specific stressors.