Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of hypercapnia on plasma renin concentration and blood pressure were studied in anaesthetized dogs, untreated and after pretreatment with guanethidine, propranolol or prazosin. An increase in plasma renin concentration which accompanied hypercapnia in untreated dogs was completely suppressed by pretreatment with guanethidine or propranolol. Prazosin significantly reduced but did not abolish renin release during hypercapnia. The pressor response normally occurring during hypercapnia was abolished by propranolol and reversed by guanethidine and prazosin.
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PMID:Participation of the sympathetic and the renin--angiotensin systems in blood pressure control during hypercapnia in the anaesthetized dog. 2 75

Twenty-two chronic hemodialysis patients with hypertension were treated with prazosin. Eight patients had volume-responsive hypertension, 11 volume-indpendent, and 3 high-renin hypertension. Blood pressure fell in all volume-responsive patients from a predialysis level of 175 +/- 5/100 +/- 3 to 148 +/- 4/75 +/- 3 mm Hg (p less than 0.001) after 3 months of therapy. Prazosin alone was effective in volume responsive patients at a dose of 5 +/- 1.0 mg daily. The blood pressure fell in volume-indpendent patients from 192 +/- 7/105 +/- 2 mm Hg predialysis to 155 +/- 6/80 +/- 3 after 3 months (p less than 0.001). Two were controlled on prazosin alone at a dose of 12 +/- 2 mg daily. Nine required 27 +/- 5 mg of prazosin daily as well as additional antihypertensive treatment. The blood pressure fell from 183 +/- 3/109 +/- 6 mm Hg predialysis to 173 +/- 17/85 +/- 3 mm Hg in high-renin patients after 3 months. One patient was controlled on 40 mg of prazosin daily. Two required 40 mg of prazosin daily as well as additional antihypertensive medication. Eleven patients described transient dizziness within the first month of therapy. One patient had recurrent syncope necessitating prazosin withdrawal; Prazosin is an effective antihypertensive agent which can be used in all types of hypertensive dialysis patients either alone or in combination with minimal side effects.
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PMID:Effects of prazosin in the control of blood pressure in hypertensive dialysis patients. 9 39

In a single-blind comparative study of the cases of 30 moderately hypertensive patients, clonidine hydrochloride and prazosin hydrochloride had similar effectiveness in lowering blood pressure. Neither agent had significant effects on the renin-aldosterone axis. Addition of polythiazide to prazosin and chlorthalidone to clonidine notably increased the antihypertensive effect of both drugs. Serum cholesterol levels were observed to decrease when prazosin and clonidine were given and to rise when the diuretics were added to the regimen. The patients treated with clonidine were troubled by side effects, particularly drowsiness and dry mouth. Prazosin was better tolerated, with side effects tending to diminish with time. The "first-dose" effect was seen in two patients given prazosin, but it did not limit treatment. Both diuretics induced notable hypokalemia.
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PMID:Prazosin and clonidine for moderately severe hypertension. 36 88

1. The effects of intravenous (i.v.) administration of the vasodilator drugs prazosin or diazoxide on blood pressure and plasma renin activity were evaluated in the anaesthetized dog. 2. Prazosin and diazoxide both induced a rapid reduction in the mean arterial pressure to 73% and 75% of control values respectively. 3. Prazosin lowered plasma renin activity to 62% (P less than 0-025) of the control value whereas diazoxide raised plasma renin activity to 178% (P less than 0.05) of the control value. 4. The combination of vasodilatation and low renin activity observed following the administration of prazosin is unique, and may have clinical significance if these factors reduce the vascular complications of hypertension.
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PMID:Differing effects of the vasodilator drugs, prazosin and diazoxide on plasma renin activity in the dog. 97 13

Prazosin, a novel antihypertensive agent, and hydrallazine have been compared in renal hypertensive dogs. I.v. prazosin (0.1 mg/kg) produced greater falls in blood pressure than hydrallazine (1 mg/kg i.v.) but, in contrast to hydrallazine, did not cause any significant alteration in heart rate or plasma renin activity in these animals. When given orally, prazosin (0.1 mg/kg) produced falls in blood pressure equivalent to those observed with i.v. hydrallazine (1 mg/kg) again without significant tachycardia or plasma renin activation.
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PMID:A comparsion of the effects of prazosin and hydrallazine on blood pressure, heart rate and plasma renin activity in conscious renal hypertensive dogs. 112 33

The effect of the selective 5-HT2 agonist (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI) on arterial pressure (AP), heart rate (HR), renal blood flow (RBF) and plasma renin activity (PRA) was determined in conscious rats. DOI increased AP and PRA, but decreased HR and RBF. All responses to DOI were abolished by central (LY 53857) or peripheral (xylamidine) 5-HT2 antagonists. Prazosin did not alter the AP or HR response to DOI. Chlorisondamine abolished the bradycardia but slightly increased the hypertension produced by DOI, while enalapril attenuated the pressor response. No further reduction was produced by the combination of enalapril and prazosin. Propranolol attenuated but did not eliminate the renin response, and blocked the bradycardia elicited by DOI. The data suggest that DOI activates 5-HT2 receptors located on vascular smooth muscle and/or the circumventricular organs of the brain to: (1) increase AP and reflexly decrease HR, (2) decrease RBF and (3) increase PRA. The hypertension is mediated by angiotensin II and direct vascular effects whereas the increase in PRA is mediated by an interaction of increased sympathetic nerve activity and decreased renal perfusion pressure.
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PMID:Hemodynamic and renin responses to (+-)-DOI, a selective 5-HT2 receptor agonist, in conscious rats. 218 26

The specific competitive alpha 1-postsynaptic blocking action and haemodynamic effects of prazosin (Minipress) have been summarized. Prazosin causes dilatation of arterioles and veins, reduces total peripheral resistance as well as preload and afterload. Cardiac output does not change at rest, stroke volume and subsequent cardiac output increase during exercise. The changes in heart rate have non-significant. It does not cause sympathetic counter-regulation, plasma renin activity does not increase, aldosterone level decreases, salt- and fluid retention may rarely be observed. It does not provoke angina. The authors report on the results of their examinations with the first dose of prazosin in 61 patients (in 33 cases by the double-blind cross-over method by placebo control), and summarize the observations made with the drug in long-term treatment in Hungary. The authors and other teams used prazosin as a long-term treatment (of approximately 3 months) in combination with other drugs in a total of 344 patients, and as monotherapy in 159 patients. In the course of combination treatment side-effects were observed in 15% of the patients (dizziness, headache, weakness, occasionally palpitation). During monotherapy, side-effects occurred in 12% of the patients (tachycardia, headache, weakness, dizziness). Hungarian results confirm the usefulness of prazosin in all stages of hypertension. It is effective in 30-35% of the cases as a monotherapy (this rate is congruent with the efficacy of beta-blockers, calcium antagonists and antihypertensive drugs of central action). Earlier prazosin had been used as a third agent in combination treatment of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of the action of Minipress. Examinations in hypertension. 257 64

Effects of intrarenal infusions of prazosin (0.7 microgram/kg/min), yohimbine (1 microgram/kg/min), propranolol (4 micrograms/kg/min) and sulpiride (20 micrograms/kg/min) on renal prostaglandin (PG) E2 and renin release in response to renal nerve stimulation (RNS) were examined in anesthetized dogs. RNS (2.5-5 Hz, for 10 min) decreased renal blood flow and increased both PGE2 and renin secretion rates. The blood flow response was inhibited by prazosin but not by other antagonists. Prazosin and propranolol, but not yohimbine or sulpiride, attenuated the renin response. However, none of these antagonists affected the PGE2 response. The results suggest that the RNS-induced renin release is mediated by alpha adrenoceptors, which seem to be alpha-1 type, and beta adrenoceptors, but the RNS-induced PGE2 release is not mediated by these adrenoceptors. Renal dopaminergic component may play no significant role in the RNS-induced PGE2 or renin release.
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PMID:Effects of blockades of alpha and beta adrenoceptors and dopamine receptors on renal nerve stimulation-induced prostaglandin E2 and renin release in anesthetized dogs. 286 53

1. Intra-arterial blood pressures and heart rates were recorded in conscious, unrestrained, Long Evans and Brattleboro rats receiving sequential, continuous administrations of selective alpha 1- (prazosin) and alpha 2- (idazoxan) adrenoceptor antagonists. The same protocols were also run in the presence of ICI 118551 (a selective antagonist of beta 2-adrenoceptors). 2. Prazosin and idazoxan caused large, but transient, hypotensions in Long Evans and Brattleboro rats. In the continued presence of both drugs there were marked, intermittent, depressor episodes and tachycardias in both strains of rat. 3. In the presence of low or high doses of ICI 118551 the hypotensive responses to prazosin and idazoxan were markedly reduced in both strains of rat and blood pressures showed little variability, although intermittent tachycardias still occurred. 4. In adrenal-demedullated Long Evans rats, the hypotensive responses to prazosin and idazoxan were attenuated and in the presence of both drugs, blood pressure was relatively steady, although intermittent tachycardias still occurred. 5. In the presence of prazosin and idazoxan, when a depressor episode was not occurring, administration of captopril caused hypotension in Long Evans and Brattleboro rats. In the latter, the reduction in blood pressure was sustained, whereas there was a recovery in blood pressure in Long Evans rats. This recovery was punctuated by depressor episodes, and was abolished by a V1-receptor antagonist (d(CH2)5DAVP). 6. Long Evans rats given two primed doses of the non-selective alpha-adrenoceptor antagonist, phentolamine, exhibited variation in blood pressure similar to that seen in the presence of prazosin and idazoxan. As in the latter case, blood pressure variability was inhibited by the beta 2-adrenoceptor antagonist, ICI 118551. 7. Administration of idazoxan into a lateral ventricle in Long Evans rats receiving phenoxybenzamine intravenously did not cause blood pressure instability. However, intravenous administration of idazoxan in the same animals produced intermittent depressor episodes and tachycardias similar to those seen in the presence of prazosin and idazoxan. 8. The simplest explanation of the results is that beta 2-adrenoceptor-mediated depressor mechanisms contribute to the hypotensive responses to alpha 1- and alpha 2-adrenoceptor antagonism. Furthermore, in the presence of adequate peripheral alpha 1- and alpha 2-adrenoceptor antagonism, blood pressure may be maintained by the renin-angiotensin system and vasopressin (although it is only when the former system has been antagonized that a clear-cut pressor action of vasopressin is apparent). Under these conditions, blood pressure maintenance is interrupted by intermittent depressor episodes that are largely due to adrenal medullary activation.
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PMID:Involvement of beta 2-adrenoceptor-mediated mechanisms in the cardiovascular responses to alpha 1- and alpha 2-adrenoceptor antagonism in conscious, unrestrained, Long Evans and Brattleboro rats. 289 80

Long-term treatment of hypertensive rats with arterial vasodilators may further increase left ventricular hypertrophy. Since left ventricular hypertrophy may be an important determinant of outcome in hypertension, the long-term effects of arterial vasodilation with hydralazine on left ventricular mass and function were compared with those of an alternative third-line drug, the alpha1 blocker prazosin, in patients still hypertensive despite combined diuretic and beta blocker therapy. A single-blind, randomized, two-group parallel design was employed. Both treatments induced a sustained antihypertensive effect, with hydralazine showing more effect on supine blood pressure, and prazosin having more effect on standing pressure. Heart rate, cardiac output, and volume status showed only minor changes. Plasma norepinephrine showed a sustained increase when measured in both the supine and standing positions, but the increases were similar for the two treatments. Supine and standing plasma renin activity increased only during long-term treatment with hydralazine. Prazosin induced a progressive decrease in left ventricular mass over time (-34 +/- 15 g/m2 at 12 months), but hydralazine did not (-9 +/- 10 g/m2 after 12 months). Stepwise regression indicated that a decrease in systolic blood pressure was associated with a decrease in left ventricular mass with both treatments, but an increase in plasma norepinephrine was associated with an increase in left ventricular mass only with hydralazine, suggesting that increased sympathetic activity may affect left ventricular mass via cardiac alpha1 receptors. Thus, if regression of left ventricular hypertrophy is a worthwhile therapeutic goal, hydralazine and analogous arterial vasodilators are not drugs of choice.
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PMID:Vasodilators and regression of left ventricular hypertrophy. Hydralazine versus prazosin in hypertensive humans. 295 39


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