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

Angiotensin converting enzyme inhibitors were developed to prevent the in vivo generation of angiotensin II and thereby to reduce peripheral vasoconstriction. However, these compounds exert some additional effects that may or may not be angiotensin dependent. These include potential sodium diuresis, bradykinin accumulation, prostaglandin release, blunting of sympathetic activity, parasympathomimetic actions, central effects, redistribution of blood flow toward some particularly important organs. Only the comprehensive assessment of the many complex interactions that exist between the renin-angiotensin and several other regulatory systems reveals the complete therapeutic profile of this class of pharmacologic agents.
 ...
PMID:Effects of angiotensin converting enzyme inhibition: a clinical point of view. 241 18

A fall in blood pressure occurs, in most patients, within a few hours of a single dose of an angiotensin converting enzyme (ACE) inhibitor. While a serious fall in pressure is unusual in previously untreated essential hypertension, some patients are at risk of severe first-dose hypotension. These include those with treated heart failure, severe hypertension on polypharmacy, 'renin-dependent' renovascular hypertension and the occasional elderly patient. In such groups of patients the incidence of severe, symptomatic first-dose hypotension approaches 10%. This effect is not specific for ACE inhibitor therapy and may well occur as frequently with other drugs in such patients. First-dose hypotension may not be accompanied by tachycardia, possibly as a result of a parasympathomimetic action that may contribute to the first-dose effect. It is generally not possible to predict patients at risk, although plasma renin and angiotensin II concentrations show a modest positive correlation with the initial fall in blood pressure. The maximum initial hypotensive effect of ACE inhibitors is not clearly dose related but the duration of effect may be. Therefore such drugs should be started at minimum effective dosage. High-risk patients should be observed closely for at least 6 h. Symptomatic hypotension usually responds to supine rest although infusion of angiotensin II, atropine and occasionally saline may be required.
 ...
PMID:Angiotensin converting enzyme inhibitors in the clinic: first-dose hypotension. 282 78

Angiotensin converting enzyme inhibitors were developed to prevent the in vivo generation of angiotensin II and thereby to reduce peripheral vasoconstriction. However, these compounds exert some additional effects that may or may not be angiotensin dependent. These include potential sodium diuresis, bradykinin accumulation, prostaglandin release, blunting of sympathetic activity, parasympathomimetic actions, central effects, redistribution of blood flow toward some particularly important organs. Only the comprehensive assessment of the many complex interactions that exist between the renin-angiotensin and several other regulatory systems reveals the complete therapeutic profile of this class of pharmacologic agents.
 ...
PMID:Pharmacology of converting enzyme inhibitors. 303 88

Acute administration of the parasympathomimetic agent, bethanechol, at 2, 4, 8 and 12 mg/kg body wt, IP, induced drinking and increased urine output of rats in a dose-dependent fashion. The first significant increases in both water intake and urine output above that of controls occurred when 4 mg/kg was administered. The drinking and increased urine output in response to administration of 8 mg bethanechol/kg was inhibited by atropine sulfate (3 and 6 mg/kg, IP). In addition, the beta-adrenergic antagonist, propranolol (6 mg/kg, IP, administered 30 min prior to treatment with bethanechol), inhibited bethanechol (8 mg/kg, IP)-induced drinking. Urine output, however, was unaffected by propranolol. Further, the angiotensin I converting enzyme inhibitor, captopril, inhibited significantly the drinking response, but not the increased urine output, accompanying administration of bethanechol (8 mg/kg). The effect of bethanechol and the beta-adrenergic agonist, isoproterenol (25 micrograms/kg) separately and in combination, on water intake was also studied. Both compounds increased water intake but they exerted no interactive effect when administered simultaneously. Administration of bethanechol (8 mg/kg) to conscious rats was also accompanied by a significant reduction in both mean blood pressure and heart rate that reached minimal levels within 10 min after treatment. Both responses had returned to control level by one hr after treatment. These results suggest that bethanechol induces drinking in rats by way of the renin-angiotensin system.
 ...
PMID:Bethanechol-induced water intake in rats: possible mechanisms of induction. 612 43