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)

Renal prostaglandins (PG) appear to mediate renin release due to stimulation of the intrarenal baroreceptor, but not that due to activation of the macula densa. However, as the role of PG in sympathetically mediated renin release remains unclear, a possible interrelationship between these factors was examined in conscious rats. Hydralazine increased the serum renin levels from 3.1+/-0.8 to 16.7+/-3.0 ng/ml per h at a dose of 1 mg/kg. Indomethacin (5 mg/kg) suppressed urinary PGE(2) and PGF(2alpha) excretion by 89 and 74%, respectively, arachidonate hypotension by 82%, and inhibited the elevated renin levels from hydralazine by 100% without altering the hypotensive effect of the drug. Another PG synthetase inhibitor, meclofenamate, was also effective in attenuating hydralazine-induced renin release, urinary PGE(2) and PGF(2alpha) excretion, and arachidonate hypotension. Isoproterenol, a nonselective beta-adrenergic agonist, increased heart rate, lowered blood pressure, and also stimulated the release of renin when administered intraperitoneally. However, intrarenal infusion of the drug only resulted in increased renin release. Indomethacin inhibited isoproterenol-induced renin release by 66 and 67%, respectively, without altering the hemodynamic effects associated with the intraperitoneal administration of the drug. The selective beta(1) agonist, H133/22, increased the release of renin and heart rate in a dose-related manner without altering blood pressure. H133/22-induced renin release was inhibited by 80% by indomethacin pretreatment. Finally, intrarenal infusions of dibutyryl cyclic AMP (3 mg/kg per min) increased the serum activity from 4.1+/-0.2 to 20.4+/-3.9 ng/ml per h without altering mean arterial pressure. Indomethacin inhibited this renin response to dibutyryl cyclic AMP by 96%. Thus, renal PG appear to be important mediators of sympathetically stimulated renin release acting as a site distal to the beta-adrenergic receptor.
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PMID:Role of renal prostaglandins in sympathetically mediated renin relase in the rat. 3 56

The role of cyclic AMP in the regulation of renin release (RR) was studied in isolated rat kidneys, which were perfused at constant pressure in a single-pass system with a modified Krebs-henseleit solution. Isoproterenol (IP) (2 x 10(-9) to 2 x 10(-6) M) and 3-isobutyl-1-methyl-xanthine (IBMX) (4 x 10(-7) to 7 x 10(-5) M) induced a dose-dependent increase of renal perfusate flow, glomerular filtration rate and urinary sodium excretion. RR was stimulated up to 10-fold above control values within 5 min. At the lowest concentrations IP stimulated RR, but did not affect renal haemodynamics. When IP and IBMX were administered concomitantly, a supraadditive stimulation of RR was observed. Dibutyryl-cAMP (db-cAMP) and 8-Br-cGMP (10(-6) to 10(-4) M) produced a similar dose-dependent vasodilation and natriuresis, but differed in their action on RR. Within 15 min after the start of the infusion, db-cAMP increased RR up to 4-fold, whereas 8-Br-cGMP was without an effect. These results suggest that IP, IBMX and db-cAMP stimulated RR by increasing the concentrations of cAMP in the epitheloid cells and independently of changes in renal haemodynamics and sodium excretion.
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PMID:Role of cyclic AMP in the regulation of renin release from the isolated perfused rat kidney. 8 27

The intrarenal mechanisms of renin release were studied in the isolated perfused rabbit kidney during stimulation by isoproterenol, 0.01 mug/kg per min, and by theophylline, 0.87 mg/kg per min. In the absence of urinary flow during the early stages of perfusion, isoproterenol caused a 17% increase of renal vein serum renin concentration (RVSRC) (P less than 0.001) without changing renal blood flow, renal vascular resistance, or serum potassium. dl-Propranolol, 2.0 mg/kg per min. abolished this isoproterenol-induced renin release. A moderate reduction in perfusion pressure prior to the infusion of isoproterenol resulted in a marked additional stimulation of renin release. Studies during and following ureteral occlusion demonstrated that theophylline stimulates renin release by decreasing renal vascular resistance, whereas the concomitant increase in sodium transport to the macula densa exerted an opposite effect. dl-Propranolol did not affect theophylline-induced renin secretion. It is concluded that single exogenous stimuli may activate more than one intrarenal mechanism simultaneously. Isoproterenol has a direct renin-stimulatory effect on intrarenal beta-adrenergic receptors that may be reinforced by baroreceptor stimulation. Theophylline stimulates renin via a baroreceptor mechanism, with simultaneous renin suppression via a sodium-macula densa effect.
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PMID:Renin stimulation by isoproterenol and theophylline in the isolated perfused kidney. 19 Sep 4

The beta-sympathomimetic amine isoprenaline increases the plasma renin concentration by a stimulation of beta-receptors which control renin release. Isoprenaline also lowers systemic blood pressure and causes a reflex-mediated activation of the sympathetic nervous system. In these investigations it has been tested to see whether the catecholamines released by this activation modulate renin release by stimulation of certain alpha-receptors. Pretreatment of rats with reserpine or with the ganglionic blocking agent Trimethidinium enhanced the increase in plasma renin concentration induced by isoprenaline. So did pretreatment with the irreversible alpha-receptor antagonist phenoxybenzamine. Renal denervation also increased the effect of isoprenaline on plasma renin concentration. It is concluded that catecholamines released from the sympathetic nervous system can decrease renin secretion by an activation of certain alpha-receptors. The sympathetic nervous system may thus exert control of renin release by beta-receptors which stimulate and by alpha-receptors which diminish renin secretion.
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PMID:[Double controlled regulation of renin release by the sympathetic nervous system. Stimulation via beta receptors and inhibition via alpha receptors]. 19 32

The presence of renin or renin-like activity (RLA) was demonstrated in human eccrine sweat incubated with purified sheep angiotensinogen, using rat bioassay and angiotensin I radioimmunoassay. Following cholinergic stimulation, sweat RLA was found to range between 0 (unmeasurable) and 266 ng/ml.h, i.e. RLA-values of sweat can be about 10 times higher than those of plasma. Therefore, renin synthesis in sweat glands could be assumed. RLA following activation of beta-adrenergic receptors by the administration of isoprenaline (Aludrin) did not exceed the mean values obtained by cholinergic activation. After beta-adrenergic receptor blockade by propranolol (Dociton), RLA became unmeasurably low. Higher RLA-values were found after local injection of dibutyryl-c-AMP (90--210 ng/ml.h). The results indicate a beta-adrenergic regulation of RLA-release in human sweat glands. Human sweat glands appear to be useful for studying extrarenal renin release.
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PMID:Renin-like (angiotensinogenase) activity in human eccrine sweat. 21 51

1. Isoprenaline hydrochloride injected subcutaneously in rats given a choice test of 1.8% NaCl and water, first induced saline intake which started immediately and was almost concluded in 15 min, followed by a copious water intake. When either saline or water were given in a separate test, saline intake surpassed the water intake in the first 15 min.2. The delay of 15, 30 or 60 min after injection of isoprenaline, 100 mug/kg, before drinking was allowed, significantly reduced saline intake but did not modify the amount of water subsequently drunk.3. Isoprenaline caused a sudden drop in arterial blood pressure, the extent and duration depending on the dose. The time of maximum drop 3-4 min after injection coincided with the time the rat drank salt.4. Isoprenaline-induced saline drinking was significantly reduced after bilateral nephrectomy but water intake was unaffected.5. The beta-adrenoceptor blocking agent, propranolol, inhibited isoprenaline-induced NaCl and water intake, while the alpha-adrenoceptor antagonist phenoxybenzamine abolished isoprenaline-induced NaCl intake and enhanced water intake.6. Saralasin acetate (P-113), a competitive inhibitor of angiotensin II, given into the third brain ventricle, prevented the isoprenaline-induced NaCl and water intake as well as angiotensin II-induced drinking. The angiotensin converting enzyme inhibitor SQ-20881 reduced the isoprenaline-induced NaCl and water intake.7. In conclusion, hypotension might be a component of salt drinking evoked by isoprenaline although the dipsogenic action of beta-stimulation is mainly due to endogenous renin-angiotensin activation.
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PMID:Drinking behaviour in rats treated with isoprenaline, angiotensin II or angiotensin antagonists. 23 Nov

The effects of selective beta adrenergic receptor stimulation with isoproterenol (3 X 10(-8) M) and of beta adrenergic blockade with pindolol (3 X 10(-5) M) on the renin release in vitro were investigated in incubated canine and rat kidney slices. Bioassay was used to measure the renin content of the tissue samples and incubation media; renin content in the canine incubation medium was measured also by radioimmunoassay. Isoproterenol in a concentration of 3 X 10(-8) M brought about a significant increase in the renin content of the incubation media as well as the tissue slices obtained from canine kidney, however, there was no change in these parameters under similar conditions if rat kidneys were incubated. Pindolol, on the other hand, in a concentration of 3 X 10(-5) M caused a significant decrease in the renin release from as well as in the renin content of the rat kidney slices, while canine kidney slices failed to respond to the same dose of the drug. The differences between the two species is suggested to be due to the differences in basal renin levels.
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PMID:Species differences in the effect of isoproterenol and pindolol on renin release in vitro. 39 60

The association between fetal arterial pressure and fetal plasma renin activity (PRA) was studied in 30 fetal lambs prepared acutely, but studied in utero. There was a negative correlation between resting fetal arterial pressure and resting fetal PRA (p less than 0.05). Fetal hypotension caused by intravenous infusion of sodium nitroprusside was associated with increases in fetal PRA. Fetal hypertension caused by intravenous infusion of phenylephrine to the fetus was associated with a decrease in fetal PRA. Maternal hypotension caused by infusion of sodium nitroprusside to the mother, and maternal hypertension caused by maternal infusion of phenylephrine caused an increase in fetal blood pressure and a fall in fetal PRA. It is concluded that the hypertensive response of the fetus to these changes in maternal blood pressure was not initiated by the fetal renin-angiotensin system. Isoprenaline caused a rise in fetal PRA. In 11 of 28 infusions this increase in fetal PRA occurred even though diastolic pressure was increased. It is concluded that there is a beta-adrenergic receptor in the fetal kidney which can release renin. The increase in fetal PRA with intravenous isoprenaline was blocked by propanolol. Infusions of adrenaline were not associated with increases in fetal PRA.
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PMID:The actions of vasoactive drugs on fetal and maternal plasma renin activity. 42 Aug 84

1. In nephrectomized rats, S.C. (0.12 mg. kg body wt.(-1)) or intracerebroventricular (I.C.V.: 0.03 mg. kg(-1)), isoprenaline failed to elicit drinking. However, when preceded (5-20 min) by a non-dipsogenic dose of I.V. pig renin, S.C. isoprenaline induced a marked, and I.C.V. isoprenaline a smaller drinking response. 2 hr after I.V. renin, S.C. isoprenaline no longer caused drinking.2. Pig renin did not enhance drinking in response to 0.12 mg. kg(-1) isoprenaline S.C. in intact or sham-operated rats.3. Isoprenaline (0.12 mg. kg body wt.(-1), S.C.) caused a larger fall of blood pressure in unanaesthetized nephrectomized than in intact unanaesthetized rats, but it was not the resulting hypotension that interfered with the nephrectomized rats' ability to drink, since intact rats with similar falls in blood pressure drank avidly in response to large doses of isoprenaline.4. Since the rate of inactivation of pig renin in nephrectomized rats was not modified by isoprenaline, drinking in nephrectomized animals in response to renin+isoprenaline was not attributable to increased plasma renin levels.5. Since isoprenaline induces drinking in the presence of circulating renin, but in the absence of renin release from kidneys, renin plays a permissive role in isoprenaline-induced drinking. Angiotensin and isoprenaline may interact at the level of intracranial receptors.
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PMID:The role of circulating renin in drinking in response to isoprenaline. 48 Feb 53

Isoproterenol is a potent dipsogen and antidiuretic agent. It also stimulates the release of renin from the kidney. Evidence is presented to substantiate the view that the drinking and increased vasopressin release that follow the systemic injection of a small dose of isoproterenol are mediated via increased activity of the renin-angiotensin system. Larger doses of isoproterenol, which have profound effects on the cardiovascular system, cause drinking and vasopressin release by mechanisms that do not depend solely on the renin-angiotensin system. Other experiments discussed do not support the hypothesis that hypothalamic beta-adrenergic neurons are important in facilitating thirst. Low doses of isoproterenol are more effective in causing drinking and vasopressin release when given peripherally rather than centrally. Evidence is discussed that supports the view that isoproterenol given centrally leaks into the periphery and causes release of renin and subsequent stimulation of drinking and vasopressin release.
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PMID:Beta-adrenergic thirst and its relation to the renin-angiotensin system. 71 May 89


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