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 effect of i.v. infused (asp1-beta-amid, val5)-angiotensin II (1.0 mug/kg min), octapressin (phe2, lys8-vasopressin) (10.0 mU/kg min) and of the alpha-sympathomimetic amine phenylephrine (40.0 mug/kg min) on the stimulation of renin secretion by furosemide (10.0 mg/kg i.v.) was investigated. The vasoconstrictors abolished the renin release induced by forosemide. Studies on the clearance of p-aminohippuric acid (PAH) (i.e. renal plasma flow) showed that the action of the vasoconstrictors cannot be explained by a decrease in access of furosemide to its intrarenal sites of action. The mechanism of the suppressive action of the vasoconstrictors on renin release is discussed.
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PMID:Inhibition of furosemide-induced renin release by vasoconstrictors. 118 24

The mechanism of the increase in plasma renin concentration caused by the beta-sympathomimetic agent isoprenaline has been further investigated. Rats were pretreated by occluding the left renal artery for 2 hrs, thus rendering the macula densa cells of this kidney nonfunctioning. After contralateral nephrectomy infusion of isoprenaline (1.5 mug/kg min) still caused a strong increase in plasma renin concentration. This increase was significantly suppressed by simultaneous infusion of angiotensin II (1.0 mug/kg min). The alpha-sympathomimetic amine phenylephrine (60 mug/kg min) or octapressin (10 mU/kg min). The results exclude any mediator-role of the macula densa receptors in the isoprenaline-induced release of renin. The possibility of a stimulation of renin release via the baroreceptors or a direct "secretomotoric" action of isoprenaline is discussed.
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PMID:Suppression of isoprenaline-induced increase in plasma renin concentration by vasoconstrictors in rats with nonfunctioning Macula densa. 118 25

In dogs, plasma renin activity (PRA) was increased by anesthesia, by hypercapnia and by extreme hypoxia (paO2 47.6 mm Hg). Relatively moderate hypoxia (paO2 47.6 mm Hg) and artificial respiration had no appreciable influence on PRA. It appears that the sympathomimetic stimulus of CO2 has an important bearing on PRA.
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PMID:[Proceedings: Experimentally induced effects on the plasma renin activity]. 121 77

The renin-angiotensin system consists of two main enzymes, renin and angiotensin-converting enzyme, which lead to the formation of angiotensin-II. Angiotensin-II is a potent vasoconstrictor and stimulates the production of aldosterone. In this study we examined the effect of ACTH, potassium, (Bu)2cAMP (dbcAMP), and catecholamines on the adrenal renin-angiotensin system. To study the production of renin and aldosterone in vitro, we developed a monolayer culture of bovine zona glomerulosa cells in serum-free medium. Collagenase-dispersed zona glomerulosa cells were incubated in Pasadena Foundation for Medical Research-4 medium containing 10% fetal calf serum for 72 h, and the medium was replaced with serum-free medium for the next 24 h of the experimental period. The cells during this 24 h were exposed to various doses of ACTH, potassium, dbcAMP, and sympathomimetic agents. ACTH and dbcAMP stimulated aldosterone secretion, and this secretion was associated with an increase in renin activity in cells and medium. Aldosterone was also stimulated by high doses of potassium, and potassium had a stimulatory effect on the secretion of renin in medium. Catecholamines had a weak stimulating effect on aldosterone secretion and were potent stimulators of adrenal renin activity in cells and medium. Dopamine had no significant effect on basal aldosterone secretion or renin activity in cells and medium. In conclusion, these data indicate that adrenal renin is synthesized in bovine zona glomerulosa cells in vitro, and that ACTH and dbcAMP stimulate adrenal renin and aldosterone production. Furthermore, adrenal renin, like renal renin, may be under the control of the sympathetic nervous system.
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PMID:Regulation of the adrenal renin angiotensin system in cultured bovine zona glomerulosa cells: effect of catecholamines. 131 45

Factors that can influence cardiovascular growth are becoming increasingly important for our understanding of such complex diseases as cardiac hypertrophy, coronary artery disease, atherosclerosis, and hypertension. Several proto-oncogenes were found to be involved in the regulation of abnormal cell growth in cardiovascular disease. It is also evident that some peptide hormones, which are well known to be involved in blood pressure control, may play a role as growth modulators. Angiotensin II is one such peptide. It elevates blood pressure through its direct vasoconstrictor, sympathomimetic, and (through release of aldosterone) sodium-retaining activity but also appears to have mitogenic actions. Interestingly, all components of the renin-angiotensin system were found locally in cardiovascular tissues. The question remains whether angiotensin can act directly as a growth factor or whether it does so indirectly by influencing or modulating cell growth factors. A better understanding of the renin-angiotensin system as a direct or indirect mediator for cardiovascular hypertrophy would offer new and interesting insights into the pathophysiology of hypertension and possibly novel options for the treatment of cardiovascular disease.
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PMID:The molecular basis of cardiovascular hypertrophy: the role of the renin-angiotensin system. 138 95

Various beta-blockers possessing similar antihypertensive potency have been found to differ widely with regard to their influence on blood pressure-regulating factors such as cardiac output and plasma levels of renin or norepinephrine. Recently, beta-blocker-induced stimulation of circulating atrial natriuretic factor (ANF) was reported. Blood pressure is determined not only by levels of vasoconstrictive factors but also by tissue reactivity. To investigate these aspects, we assessed the cardiovascular responsiveness to norepinephrine and angiotensin II, plasma levels of catecholamines, angiotensin II, ANF and aldosterone and the body sodium-blood volume state of 15 patients with essential hypertension (mean age +/- s.e.m., 42 +/- 3 years) and 12 normal control subjects (41 +/- 5 years), first on placebo and then after 4 weeks of intervention with carteolol, a non-selective beta-adrenergic antagonist with intrinsic sympathomimetic activity. Compared with placebo, carteolol decreased resting plasma norepinephrine in both groups while plasma norepinephrine-blood pressure response curves were shifted to the left, their slopes increased and norepinephrine pressor doses decreased (P less than 0.05 to less than 0.001). Chronotropic responses to isoproterenol were abolished but negative chronotropic responses to a norepinephrine-induced 20 mmHg rise in diastolic blood pressure were unaltered. Plasma norepinephrine clearance in the supine position was slightly decreased in hypertensive and unchanged in normal subjects. Supine and upright blood pressure was lowered (P less than 0.05 to 0.001) in the hypertensive while upright systolic blood pressure only decreased in the normal group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of noradrenergic but not angiotensinergic blood pressure control by beta-blockade with carteolol. 166 63

Circulating plasma concentrations of norepinephrine, renin, angiotensin and vasopressin are increased in congestive heart failure. By increasing ventricular afterload, heart failure is further worsened, which in turn--in a vicious cycle--stimulates neurohumoral vasoconstrictor mechanisms. Furthermore, because of the compensatory but excessive stimulation of the sympathomimetic system, a down-regulation and desensitization particularly of the myocardial beta 1 receptors and depletion of myocardial catecholamine occurs in chronic heart failure. These defects may be restored toward normal by interventions that attenuate the activity of the sympathetic nervous system. A direct approach to modify the excessive vasoconstriction is to administer systemic vasodilator drugs, but despite favorable short-term effects, tolerance developed to most of these drugs during long-term treatment. One reason for the loss of effectiveness is the reflex activation of the sympathetic system, which increases vasoconstrictor hormone concentrations. Activation of the renin-angiotensin system can be modified effectively by angiotensin-converting enzyme inhibitors that have shown favorable responses in patients with chronic heart failure. Beta-blocking agents interfere with endogenous sympathetic activation and have produced beneficial effects in patients with congestive cardiomyopathy. Long-term treatment is associated with up-regulation of the number of beta receptors and an improved responsiveness to catecholamines. Owing to the negative inotropic effects of beta-blocking agents, some of the patients with severe heart failure deteriorated hemodynamically and clinically. Theoretically, it should be advantageous to have a substance that combines protection against excessive beta stimulation with a mild inotropic support to prevent cardiac decompensation. This may be achieved by a selective beta 1-partial agonist like xamoterol.
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PMID:Interrupting the adaptive changes in congestive heart failure. 167 86

1. The effects of sustained moderate exercise in the sitting position on renal haemodynamics and glomerular filtration were measured in six normotensive patients with moderately impaired renal function and seven age-matched normal volunteers. 2. The changes in the effects of exercise on renal function induced by chronic cardioselective beta-adrenoceptor blockade by drugs with (epanolol) and without intrinsic sympathomimetic activity (atenolol) were examined. 3. Both beta-adrenoceptor blockers attenuated the heart rate increase with exercise, but only atenolol lowered blood pressure significantly. In resting volunteers on atenolol, associated with the fall in blood pressure there was a significant reduction in glomerular filtration rate. 4. Glomerular filtration fell significantly in all groups with exercise, and renal blood flow also fell in parallel. These changes were not influenced by drug treatment. 5. The exercise-induced rise in PRA was suppressed by atenolol but not by epanolol. 6. The renal function and haemodynamic responses to moderate exercise does not appear to be mediated by the systemic renin-angiotensin system or by beta 1-adrenoceptors.
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PMID:The effects of selective beta-adrenoceptor antagonists and partial agonist activity on renal function during exercise in normal subjects and those with moderate renal impairment. 168 67

Betablockers may be classified according to their cardio selectivity, intrinsic sympathomimetic action and direct vasodilating action. All beta blockers reduce renin plasma levels, the effect being inversely proportional to the intrinsic sympathomimetic property. The hypotensive effect is related more to vasodilation than to a decrease in cardiac output. The hypotensive action is mediated by presynaptic beta receptors which normally stimulate noradrenaline secretion by nerve endings. Adverse effects, interaction with other drugs, and effects on risk factors of beta blockers are also reviewed.
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PMID:[Pharmacology of adrenergic beta receptor blockaders]. 168 29

The presence of left ventricular hypertrophy (LVH) is of poor prognosis in essential arterial hypertension, but it may regress under antihypertensive treatment. Angiotensin-converting enzyme inhibitors, calcium antagonists, centrally acting antihypertensive agents and beta-blockers with low intrinsic sympathomimetic activity constantly reduce the left ventricular mass. This stands in contrast with diuretics and vasodilators which induce stimulation of the sympathetic and/or renin-angiotensin systems and usually have no effect on LVH. Animal experiments have shown that regression of LHV has no adverse effect on the myocardial changes aimed at correcting the LVH-associated abnormalities (collagen content, changes in isomyosins, density of beta-adrenergic receptors, etc.) and that it improves the coronary haemodynamics disturbed by LVH. In clinical practice, reducing the ventricular mass does not modify the left ventricular systolic function, usually improves the diastolic function precociously altered by LVH and seems to reduce the LVH-induced ventricular hyperexcitability. The regression of LVH under antihypertensive treatment should result in a lesser cardiovascular risk in hypertensive patients.
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PMID:[Regression of left ventricular hypertrophy with antihypertensive treatment]. 197 67


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