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)

Rat kidneys perfused in vitro released kallikrein in urine, and renin and kallikrein in the perfusate. The kallikrein was characterized by its kininogenase activity and released bradykinin from bovine and dog substrates. Inactive trypsin activatable kallikrein was present in both perfusate and urine. Kallikrein secretion in urine was influenced by changes in perfusion pressure (PP). Raising the PP strikingly increased urinary kallikrein and lowering PP reduced it. Urinary water and electrolyte output were augmented to the same extent by furosemide and mannitol administration as by raising the PP, but neither drug affected kallikrein. Isoproterenol stimulated the release of renin but not kallikrein. Stopping the oxygen supply to the perfusate suppressed kallikrein secretion in urine and renin release in the perfusate. The kidneys released ten times less kallikrein in the perfusate than in urine, and perfusate kallikrein was not influenced by changes in PP. It is concluded that in this model, changes in PP and/or renal blood flow and/or oxygen supply regulate kallikrein secretion in urine, but that this secretion is unaffected by changes in urinary output. We also conclude that kallikrein release in urine and renin release in perfusate are regulated simultaneously by renal hemodynamic changes but are not affected concomitant by beta-adrenergic stimulation or changes in distal urine composition.
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PMID:Regulation of kallikrein and renin release by the isolated perfused rat kidney. 635 42

The inhibition of renin release by angiotensin II (AII) is well documented. However, the interaction of this short loop feedback mechanism of AII with the sympathetic nervous system is still unclear. This study was designed to investigate the possible functional relationship between AII and the beta-adrenergic receptors with respect to renin release in vivo. First, the effect of propranolol on captopril-induced renin release was examined in conscious rats. Secondly, the effect of AII on isoproterenol-induced renin release was determined. Captopril (1 mg/Kg) increased plasma renin activity (PRA) from 1.6 +/- 0.3 ng/ml/hr to 4.5 +/- 0.6 ng/ml/hr (p less than 0.01). In contrast, there was no significant change in PRA in rats which received both captopril and propranolol (before 0.9 +/- 0.2 ng/ml/hr, after 1.3 +/- 0.3 ng/ml/hr). Thus, propranolol attenuated the increase in PRA caused by captopril. Isoproterenol infusion (0.1 micrograms/Kg/min) provoked a significant increase in PRA (before 1.3 +/- 0.4 ng/ml/hr, after 6.6 +/- 1.7 ng/ml/hr, p less than 0.01). AII infusion in combination with isoproterenol also increased PRA from 1.6 +/- 0.4 ng/ml/hr to 5.2 +/- 0.3 ng/ml/hr (p less than 0.01). AII in this dose did not suppress isoproterenol-induced renin release. These results suggest that the beta-adrenergic receptor mediating renin release is functionally located distal to the AII receptor in the short loop mechanism controlling renin release.
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PMID:Inhibition of captopril-induced increase in plasma renin activity by propranolol. 635 80

Rat renal slices were incubated in two different media. One was a normal K, physiological saline solution and the other a high K medium. Renin release was measured every 15 min in the presence and absence of 10(-6) M isoproterenol and also in the presence and absence of aspirin, 0.8 or 1.6 X 10(-5) M. In all experiments renin release was linear during the 75 min of incubation. Isoproterenol increased renin release by approximately 100%. This was the case even in the presence of aspirin which significantly inhibited prostaglandin release (PGE2, PGF2 alpha and 6-keto-PGF1 alpha). Nor was there any reduction in the basal secretory rate by aspirin alone. These data are taken to indicate that aspirin in pharmacological doses does not interfere with either in vitro basal release rates of renin, nor the response to B agonists. It is also suggested that B agonists do not exert their effect by stimulating prostaglandin secretion.
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PMID:Prostaglandin biosynthesis does not participate in isoproterenol-induced renin release. 637 91

To study the relationship between PGE2 and renin release from the kidney, examinations were performed on anesthetized dogs during afferent arteriolar dilation. This condition is known to increase renin release and enhance the stimulatory effects on renin release of beta-adrenergic agonists, such as isoproterenol. Afferent arteriolar dilation induced by constricting the renal artery or occluding the ureter increased PGE2 and renin release before, but not after, indomethacin administration. Isoproterenol infusion during afferent arteriolar dilation increased renin release but not PGE2 release both before and after indomethacin administration. Phenylephrine, an alpha-adrenergic agonist, which also induces afferent arteriolar dilation, increased PGE2 and renin release at control blood pressure but not when the afferent arterioles already were dilated by ureteral occlusion. We conclude that afferent arteriolar dilation caused by renal arterial constriction, ureteral occlusion or infusion of phenylephrine increases prostaglandin synthesis which stimulates renin release. The effect of isoproterenol on renin release is independent of prostaglandin synthesis.
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PMID:Relationship between PGE2 and renin release in dog kidneys. Effects of afferent arteriolar dilation and adrenergic stimulation. 638 24

The effects on in vitro renin release from rat kidney cortex of various agents which are thought to alter intracellular Ca were investigated. Incubation in Ca-free medium had no effect on basal or isoprenaline-stimulated renin release, but the addition of EDTA stimulated renin release. Angiotensin II (ANG II) and ouabain both inhibited basal and isoprenaline-stimulated renin release, and external Ca was important in this effect. Verapamil reduced the fall in basal renin release and the inhibitory effect of ANG II. In addition, verapamil blocked the inhibition by ANG II, but not by ouabain, of isoprenaline-stimulated renin release. Isoprenaline may stimulate the Na,K-ATPase leading to increased Ca efflux via Na-Ca exchange, whereas ouabain may have the opposite effect. ANG II probably stimulates Ca influx and release from intracellular stores.
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PMID:The role of calcium in the control of renin release. 644 9

Rat renal cortical slices incubated in vitro released 7.0 +/- 0.5% (mean +/- SE, n=30) of their total renin content into the incubation medium in 1 h. Isoproterenol (10-6 M), a beta-adrenergic agonist, caused a 75 +/- 17% (n=7) increase in renin release from the cortical slices. Treatment of the cortical slices with either cycloheximide or puromycin caused a significant 96.2 +/- 0.34 (n=8) or 98.5 +/- 0.3% (n=5), respectively, inhibition of protein synthesis. After protein synthesis and presumably renin synthesis was blocked with either cycloheximide or puromycin, isoproterenol was still able to increase significantly renin release from the cortical slices despite almost total blockade of protein synthesis. We conclude that a storage pool of renin content is released may exist, since 1) only 7.0 +/- 0.5% of the cortical slice renin content is released each hour, and 2) isoproterenol stimulation of renin release is not acutely dependent on renin synthesis. It is hypothesized that beta-adrenergic stimulation of renin release is elicited from a storage pool of previously synthesized renin.
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PMID:Independence of beta-adrenergic stimulation of renin release on renin synthesis. 675 5

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.
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PMID:Effect of adrenergic agonists on big and small renin. 699 Jul 82

Isoproterenol infusion (0.1 microgram/kg per min) into the renal artery of the cat induced an increase in plasma renin concentration (PRC) from 14.3 +/- 5.7 (mean +/- SE) ng angiotensin I/ml per hr to 56.8 +/- 7.7 after 70 minutes (P < 0.05) and an increase in catecholamine secretion rate from 38.7 +/- 6.0 ng/kg per 10 min to 180.0 +/- 40.0 after 70 minutes (P < 0.001). Intravenous infusion of the same dose of isoproterenol had no significant effect on adrenomedullary catecholamine secretion rate. Isoproterenol induced preferential norepinephrine release: the ratio of norepinephrine to epinephrine secretion changed from 11.5:23.7 during the control period to 130.0:40.1 70 minutes after the start of isoproterenol administration. Intrarenal infusion of propranolol (3.0 mg/kg per min) inhibited renal renin release and adrenal catecholamine secretion in response to intrarenal isoproterenol. Intravenous infusion (0.4 microgram/kg per min) of an angiotensin II antagonist [Sar1, Ileu8]angiotensin II abolished the catecholamine response to intrarenal isoproterenol infusion. It is suggested that intrarenal isoproterenol infusion stimulates renal renin release and angiotensin production which, in turn, stimulates a preferential secretion of adrenomedullary norepinephrine.
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PMID:The role of the renin-angiotensin system in mediation of adrenal catecholamine secretion in the cat induced by intrarenal beta-adrenergic stimulation. 700 44

Renal glomeruli were isolated from rat kidneys using a passive mechanical sieving technique. Suspensions of 40-50 mg glomeruli were placed in glass chambers and superfused by a modified Krebs-Ringer solution. Effluent collections of 10-min fractions were measured for renin or prostaglandin (PG) E2 concentration using radioimmunoassays. The perfusate was altered to contain either the beta-adrenergic agonist isoproterenol, angiotensin II, or arachidonic acid. Isoproterenol at 1.78 or 8.1 X 10(-4) M produced a significant release of renin, but the concentration of PGE2 was unaffected. Isoproterenol-stimulated renin release was blocked by 1.2 X 10(-4) M propranolol but was unaffected by 6.3 X 10(-6) M meclofenamate. Angiotensin II at 4 or 40 X 10(-9) M altered neither renin nor PGE2. Arachidonic acid administered at 1.6 or 16.0 X 10(-5) M produced a marked increase in PG synthesis and stimulated a significant release of renin. Treatment of glomeruli with 6.3 X 10(-6) M meclofenamate attenuated PGE2 synthesis and abolished renin release, but 1.2 X 10(-4) M propranolol had no effect on PG synthesis or the coincident release of renin. These results give direct evidence of an interrelating mechanism between renal prostaglandins and renin release that is independent of external tubular or hemodynamic stimuli and show that the beta-adrenergic pathway of renin stimulation is independent of any modifying influence exerted by prostaglandins.
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PMID:Interaction of the prostaglandin and renin-angiotensin systems in isolated rat glomeruli. 700 11

The influence of thyroidectomy on the renin-angiotensin system was studied in the rat. From 1-6 weeks after thyroidectomy, PRA and plasma renin substrate (PRS) decreased, but the plasma renin concentration remained unchanged, and the renal renin content increased. T3 injection corrected the changes in the plasma renin-angiotensin system of thyroidectomized rats within 20-40 h. After ethinylestradiol treatment, the PRS in thyroidectomized rats rose in the same proportion as that in normal rats, but remained below the normal level. After binephrectomy, on the other hand, the PRS was high, and PRS levels in normal and thyroidectomized animals were similar. Isoproterenol increased PRA and plasma renin concentration in control animals but had no effect on thyroidectomized rats. From the above results it may be concluded that angiotensinogen production is dependent on thyroid hormones and that renin release depends on beta-adrenergic receptor sensitivity to catecholamines, which is reduced by thyroidectomy. (Endocrinology 108: 647, 1981)
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PMID:The renin-angiotensin system in thyroidectomized rats. 700 61


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