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)

Changes in hemodynamic variables and renin release, induced with both alpha and beta adrenergic agonists, were studied in 5 normal men. Saline (0.9% NaCl), methoxamine (1.6 and 5.9 mug/kg/min), and isoproterenol (0.015 and 0.026 mug/kg/min) were infused individually in a random order for 30 min. Methoxamine and isoproterenol caused the predicted directionally opposite cardiovascular changes but caused nearly equal and dose-related increases in plasma renin activity, as measured by radioimmunoassay. Saline infusion had no effect. Propranolol (0.125 mg/kg) caused decreases in systolic pressure and heart rate, and a significant decrease in plasma renin activity. Propranolol prevented the renin-releasing effects of isoproterenol and methoxamine, but only the cardiovascular effects of isoproterenol. It appears that alpha or beta agonists stimulate renin release equally in man and that at least one step in renin is propranolol-sensitive. Such sensitivity may be independent of its beta receptor blocking activity.
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PMID:Alpha and beta adrenergic-induced renin release in man. 114 59

Controversy exists regarding the mechanism by which catecholamines stimulate renin secretion in vivo. A sensitive rat kidney slice system was utilized to study the direct effects of adrenergic agonists and antagonists on renin release in vitro. Catecholamines were protected from degradation by the addition of ascorbic acid to the incubation medium. Significant dose-related stimulation of renin release was observed with epinephrine and norepinephrine in concentrations from 1.5 times 10(-9) to 1.5 times 10(-7)M and with isoproterenol in concentrations from 2 times 10(-9) to 2 times 10(-7)M. No significant stimulation was seen with 10(-10)M concentrations of the three agents. Methoxamine (10(-6)M) stimulated renin release significantly (P less than 0.01). The stimulation observed with epinephrine, norepinephrine, or isoproterenol was blocked by d,l- and l-propranolol (2 times 10(-4)M) but not by d-ropranolol (2 times 10(-4)M) or phentolamine (9 times 10(-4)M). Methoxamine-induced stimulation was abolished by d,l-propranolol but not by phentolamine. These data that the in vitro kidney slice system is responsive to physiological concentrations of catecholamines when they are protected from degradation. The results further demonstrate a direct stimulatory role for beta-adrenergic agents on renin release and suggest that alpha-adrenergic effects seen in vivo are mediated indirectly by hemodynamic, vascular, or functional changes in the kidney.
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PMID:Direct effect of beta-adrenergic stimulation on renin release by the rat kidney slice in vitro. 115 20

Experiments were performed in conscious trained dogs to determine whether renal alpha-adrenergic receptors mediate stimulation or inhibition of renin release. All dogs were uninephrectomized and surgically prepared with chronically indwelling catheters in the aorta, vena cava, and remaining renal artery at least 8 days before experiment. Direct renal artery (ia) infusion of the alpha-adrenoceptor agonist phenylephrine, 0.25 or 0.50 microgram X kg-1 X min-1 for 30 min, increased plasma renin activity (PRA) to 145 +/- 13 and 212 +/- 28% of control, respectively, within 5 min of drug infusion (P less than 0.01) in conscious sodium-replete dogs. In contrast, intravenous phenylephrine infusion decreased PRA by 50% (P less than 0.001). The increase in PRA observed during ia phenylephrine infusion was prevented by renal alpha-adrenoceptor blockade with phenoxybenzamine but not by beta-adrenoceptor blockade with propranolol. Methoxamine, another alpha-adrenoceptor agonist, also increased PRA when infused ia in both sodium-replete dogs and in dogs maintained on a low-sodium diet. In dogs with renal arterial electromagnetic flowprobes, ia phenylephrine infusion increased PRA without decreasing total renal blood flow. In summary, stimulation of renal alpha-adrenoceptors increases PRA in conscious dogs. This stimulation can occur in the absence of significant changes in total renal blood flow.
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PMID:Elevation of plasma renin activity by alpha-adrenoceptor agonists in conscious dogs. 353 1

The relationship between renin release and renal prostaglandin (PG) production induced by the alpha-agonists methoxamine and alpha-methylnorepinephrine was examined in anesthetized dogs. Both intrarenal infusions of methoxamine (1, 3, and 5 micrograms/min) and alpha-methylnorepinephrine (0.37, 1, and 2 micrograms/min) resulted in a dose-dependent decrease in renal blood flow to a slight degree. Methoxamine dose-dependently increased the renin secretion rate but failed to increase the PGE2 secretion rate. In contrast, alpha-methylnorepinephrine failed to affect the renin secretion rate but dose-dependently increased the PGE2 secretion rate. The effect of methoxamine (5 micrograms/min) on renin release was abolished by the intrarenal alpha 1-adrenoceptor blockade with prazosin (3 micrograms/min) but was not affected by the intrarenal alpha 2-adrenoceptor blockade with yohimbine (30 micrograms/min). The effect of alpha-methylnorepinephrine (2 micrograms/min) on PGE2 release was abolished by yohimbine but not by prazosin. These results suggest that there is a dissociation between renin release and renal PG production induced by alpha-agonists and that renal alpha 1- and alpha 2-adrenoceptors may participate in renin and PGE2 release, respectively.
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PMID:Effects of alpha-agonist on renin and prostaglandin E2 release in anesthetized dogs. 614 93

To examine whether an alpha-adrenergic agonist, methoxamine, influences renin release solely by its haemodynamic effect, experiments were performed in anaesthetized dogs with denervated kidneys. Methoxamine was infused intrarenally at rates which reduced renal blood flow (RBF) by 30-40%. At control blood pressure, renin release rose during infusion of methoxamine from 1.4 +/- 0.7 to 31 +/- 11 microgram/min. A beta-adrenergic stimulator, isoproterenol, did not increase renin release significantly when administered alone into the renal artery, but doubled the effect of methoxamine infusion: at control blood pressure renin release rose from 0.5 +/- 0.3 to 71 +/- 17 microgram/min during combined infusion of isoproterenol and methoxamine. Mechanical constriction of the renal artery left RBF unaltered down to a renal perfusion pressure of 90 +/- 4 mmHg during methoxamine infusion, whereas the lowest autoregulating pressure in control experiments averaged 60 +/- 5 mmHg. At renal infusion pressure below the range of autoregulation, renin release was not further increased by intrarenal infusion of methoxamine. Isoproterenol infusion at low renal perfusion pressure doubled renin release, which was not significantly altered by additional infusion of methoxamine. The stimulatory effect of methoxamine on renin release at control blood pressure could be diminished but not prevented by infusing 2.9% NaCl intravenously in large amounts. These data indicate that methoxamine induces autoregulated dilation of afferent arterioles by disproportionate vasoconstriction on pre-afferent arteries. Thereby afferent arterioles are conditioned for stimulation of renin release by isoproterenol.
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PMID:Conditions for humoral alpha-adrenoceptor stimulation of renin release in anaesthetized dogs. 627 76