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)

Both inactive and active renin were released from renal cortical slices of the hog. Isoproterenol, prostaglandin E1, and dibutyryl cAMP stimulated the release of both inactive and active renin. Renal kallikrein caused selective stimulation of the release of active renin and suppressed the release of inactive renin. Bradykinin and kallidin did not stimulate renin release. The effect of kallikrein was abolished by aprotinin but not by indomethacin. These observations indicate that the effect of kallikrein is not mediated via kinin formation or prostaglandin generation. The data suggest that there may be at least two types of mechanism for renin release from hog kidney. One is of the nonselective type by which both active and inactive renin are released, as in the case of beta-adrenergic or prostaglandin stimulation. The other is a selective mechanism by which only active renin is preferentially released, as in the case of urinary or renal kallikrein stimulation.
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PMID:Release of active and inactive renin from hog renal cortical slices in vitro. 620 37

Isoprenaline bitartrate (0.5 microgram/kg/min i.v.) increased the rate of noradrenaline release into the circulation of pentobarbitone-anesthetized rabbits. This increase was much greater than that produced by an equi-hypotensive dose of the vasodilator hydralazine (0.2 mg/kg i.v.), suggesting that it was only partly due to baro-reflex activation of sympathetic nerves. This facilitatory effect of isoprenaline was also observed in the nephrectomized, pithed rabbit, with electrically stimulated sympathetic outflow, ruling out central nervous system and renin-angiotensin effects. ICI 118,551 HCl (0.3 mg/kg + 0.1 mg/kg/h i.v.) blocked the isoprenaline-induced hypotension, but did not affect the isoprenaline-induced tachycardia, suggesting that it selectively blocked beta 2-adrenoceptors. ICI 118,551 totally abolished the isoprenaline-induced increase in noradrenaline release, suggesting a beta 2-effect. Atenolol (0.3 mg/kg + 0.1 mg/kg/h) blocked the isoprenaline-induced tachycardia, a beta 1-effect, but only slightly attenuated the isoprenaline-induced increase in noradrenaline release. Atenolol by itself decreased heart rate and arterial pressure, but there was no reflex rise in the noradrenaline release rate, which suggests that atenolol impairs baroreceptor activation of sympathetic nerves. In another series of experiments, also in the pentobarbitone-anesthetized rabbit, adrenaline was released into the circulation by splanchnic nerve stimulation. This resulted in prolonged increases of adrenaline levels in heart tissue. After the plasma adrenaline levels had returned to prestimulation values, the rate of noradrenaline release into the plasma was enhanced. This increase was not observed in rabbits treated with either desipramine HCl (1 mg/kg i.v.) or propranolol HCl (2 mg/kg i.p.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Local modulation of noradrenaline release in vivo: presynaptic beta 2-adrenoceptors and endogenous adrenaline. 620 19

Using a continuous superfusion system of rat kidney cortical slices, we investigated the renin-releasing effect of prostaglandin E2 (PGE2) and its possible mechanism of action. PGE2 caused significant stimulation of renin release in a dose-dependent fashion at concentrations of 3 x 10(-6) to 10(-4) M. Isoproterenol (8 x 10(-7) M) stimulated renin release significantly, and its effect was completely abolished by propranolol (2 x 10(-5) M). PGE2-stimulated renin release was not blocked by the same dose of propranolol. Dibutyryl cAMP caused a dose-dependent increase in renin release at concentrations of 10(-5) to 5 x 10(-3) M. Theophylline (4 x 10(-3) M) had no effect on renin release, but when added to subthreshold doses of PGE2 (10(-6) M), it stimulated renin release significantly. The simultaneous addition of maximal stimulating doses of PGE2 and dibutyryl cAMP had no additive or synergistic effects. These experiments show that PGE2 causes stimulation of renin release by a direct effect on the JG cell. The renin-releasing effect of PGE2 does not depend upon the beta-adrenergic receptors but may be mediated through cAMP.
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PMID:Prostaglandin stimulation of renin release: independence of beta-adrenergic receptor activity and possible mechanism of action. 624 27

Renal prostaglandins (PGs) have been considered to be important mediators of renin release. However, the mechanism and the site of action have not been clarified. To investigate the role of PGs in the control of isoproterenol-induced renin release, we studied the effect of two inhibitors of PG synthesis, indomethacin and meclofenamate, on the renin release stimulated by isoproterenol and dibutyryl cAMP. We used an in vitro superfusion system of rat renal cortical slices. Neither indomethacin nor meclofenamate affected basal renin release. Isoproterenol (8 x 10(-7) M) increased renin and PGE2 release which was blocked by indomethacin (10(-4) M) and meclofenamate (10(-4) M). Dibutyryl cAMP stimulated renin release significantly, and this effect was not blocked by indomethacin (10(-4) M). Moreover, dibutyryl cAMP did not stimulate PGE2 release. In view of the fact that we have previously shown that PG-stimulated renin release is not blocked by propranolol and is enhanced by phosphodiesterase inhibitors, our present experiments suggest that the site of action of PGs on renin release is located between the beta-adrenergic receptor and the generation of cAMP.
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PMID:The role of renal prostaglandins in the renin response to isoproterenol in the rat in vitro. 626 Apr 59

In young subjects with normal blood pressure (N = 10) or with mild (n = 6) or moderate (n = 8) hypertension we assessed the effects of increasing doses of i.v. isoproterenol (each dose for 10 min) on systolic and diastolic blood pressure, heart rate, plasma renin activity (PRA), serum potassium and free fatty acids (FFA). Except for blood pressure, basal levels did not differ significantly between the groups. Isoproterenol induced dose-related increases in systolic blood pressure, heart rate and PRA, and dose-related decreases in diastolic blood pressure. Neither the threshold dose (i.e. the lowest dose significantly affecting these parameters), nor the changes induced by the higher doses differed between the normotensive and hypertensive subjects. Levels of serum potassium and FFA, obtained at the end of the infusion, also did not differ significantly between the groups. These results indicate, that in contrast to older and/or more severely hypertensive subjects, young subjects with mild to moderate hypertension have a peripheral beta-adrenoceptor responsiveness similar to that of normotensive controls.
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PMID:Peripheral beta-adrenoceptor responsiveness in young normotensive and hypertensive subjects. 626 69

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

These experiments were designed to study the role of calcium in the modulation of renin secretion by alpha and beta adrenoceptors. Rabbit kidneys were isolated and single-pass perfused with a modified Ringer's solution. Renal perfusion pressure was precisely controlled by an electronic servocontrol system. Tubular events were minimized by ligation of the ureter before initiating the studies. Under these conditions the predominant factor modifying renin secretion was assumed to originate directly on the juxtaglomerular cells. Isoproterenol infused at 0.1, 0.5, 1.0 and 5.0 nM/min/g of kidney weight increased renin secretion in a dose-dependent manner whereas phenylephrine infused at identical molar doses did not. In addition, phenylephrine (5.0 nM/min/g of kidney weight) blocked the usual response to isoproterenol. Removal of calcium from the perfusing medium had no effect on either the response to isoproterenol or the lack of a response to phenylephrine. On the other hand, when calcium is removed from the perfusate or when D-600, a calcium channel blocker, is added to calcium-containing medium, phenylephrine failed to block the usual response to isoproterenol. We conclude that the suppression of beta adrenoceptor stimulation of renin release by alpha adrenoceptor agonists is calcium dependent by a final mechanism as yet undefined, but probably involving movement of calcium into the juxtaglomerular cells.
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PMID:Role of calcium in the interaction of alpha and beta adrenoceptor-mediated renin release in isolated, constant pressure perfused rabbit kidneys. 631 14

Isoproterenol, dopamine, glucagon and dibutyryl cyclic AMP (DB-cAMP) increase renin release at low but not at control blood pressure. These findings suggest that autoregulated afferent arteriolar dilation is a prerequisite of renin release mediated by intracellular generation of cyclic AMP. To examine this hypothesis further the effects on renin release of theophylline, which would maintain high intracellular concentration of cAMP by inhibiting phosphodiesterase, were studied in anesthetized dogs. After inhibiting beta-adrenergic stimulation with propranolol, theophylline increased renin release significantly from 0.7 +/- 0.2 to 1.8 +/- 0.7 micrograms/min at control blood pressure and from 23 +/- 4 to 41 +/- 5 micrograms/min at a renal perfusion pressure of about 50 mmHg. The greater effect at low blood pressure occurred despite adjustment of the infusion rate of theophylline to keep arterial plasma concentration of theophylline unaltered. Isoproterenol infusion at low blood pressure raised renin release from 41 +/- 11 to 76 +/- 19 micrograms/min before and 54 +/- 13 to 108 +/- 31 micrograms/min during continuous infusion of theophylline. The renin release response to infusion of theophylline at low blood pressure was not enhanced by DB-cAMP infusion. We conclude that arteriolar dilation provides a condition for stimulation of renin release during the theophylline infusion. Theophylline infusion may augment the effect of isoproterenol on renin release by delaying the intracellular degradation of cAMP.
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PMID:Conditions for augmentation of renin release by theophylline. 631 54

To determine whether epinephrine-induced hypokalemia is due to beta2-adrenoceptor stimulation, and whether hypokalemia can occur at physiologic concentrations of the agonist, epinephrine was infused into six normal volunteers at a rate of 0.1 microgram per kilogram of body weight per minute. The circulating epinephrine concentration was increased to 1.74 +/- 0.65 ng per milliliter, plasma potassium was reduced by 0.82 +/- 0.19 meq per liter, plasma insulin fell by 12 +/- 4 mU per liter, plasma renin activity was elevated, and tachycardia occurred. Isoproterenol infused at 0.02 micrograms per kilogram per minute caused similar tachycardia (25 beats per minute) and elevation in plasma renin activity (6.0 to 6.5 ng per milliliter per hour), but no hypokalemia. The difference in responses to the two catecholamines was ascribed to the relative beta2-selectivity of epinephrine. This hypothesis was tested in six subjects given infusions of epinephrine (0.05 micrograms per kilogram per minute) after administration of either 2.5 or 5 mg of ICI 118551--a selective beta2-receptor antagonist--or placebo. After placebo, epinephrine infusion elevated the circulating epinephrine concentration and reduced plasma potassium; hypokalemia was prevented by the beta2-antagonist. This drug only partially inhibited the rises in plasma renin and glucose and the shortening of systolic time intervals; there was no tachycardia. Fifteen-fold to 30-fold increases in circulating epinephrine concentration appear to cause hypokalemia by a specific beta2-receptor effect distinct from other actions of epinephrine. This phenomenon may be of physiologic importance after severe myocardial infarction, when similar increases in plasma epinephrine have occurred.
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PMID:Hypokalemia from beta2-receptor stimulation by circulating epinephrine. 631 40

These studies were undertaken to clarify the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension (EH), and the following examinations were performed: 1) Urinary free norepinephrine and epinephrine excretion (UNEf and UEf), urinary conjugated norepinephrine and epinephrine excretion (UNEconj and UEconj), plasma norepinephrine and epinephrine concentration (PNE and PE), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 52 patients with EH, who were divided into two groups (borderline EH: b-EH, and sustained EH: s-EH), and fifteen normals (N). 2) Cardiac index (CI), total peripheral resistance index (TPRI), appearance time, mean transit time and stroke index (SI) were determined by the dye-dilution method in eight patients with b-EH, ten patients with s-EH and ten N. 3) Clonidine was administered orally in a single dose of 150 micrograms to seven patients with s-EH and three patients with b-EH, and PNE, PE and growth hormone (GH) were measured before and after the administration. 4) Isoproterenol was infused intravenously in a dose of 0.02 microgram/kg/min for 30 min to 18 patients with s-EH and six N, then plasma cyclic AMP (c-AMP) and PRA were determined before, during and after the infusion. 5) Methacholine was injected intramuscularly in a dose of 10 mg to seven N, and PNE, PE and PRA were measured before and after the injection. There were no significant differences of PNE, PE, UNEf and UEf among the three groups (b-EH, s-EH and N), but UNEconj in both b-EH and s-EH was higher than in N (b-EH: p less than 0.1, s-EH: p less than 0.05). PRA in s-EH was slightly lower not only in N but also in b-EH. PAC in b-EH and s-EH was slightly lower than in N. The difference of PAC between b-EH and s-EH was not found. CI and SI were higher than in N (p less than 0.05), but TPRI was normal. In s-EH, TPRI was slightly elevated as compared with b-EH (p less than 0.1). In s-EH, clonidine caused a significant lowering of both blood pressure and PNE with a simultaneously marked increment of GH; on the other hand, in b-EH blood pressure and PNE did not change significantly in spite of the distinct rise of GH. After the isoproterenol infusion, PRA and c-AMP increased, and there was a significant correlation between the initial level of PRA and the maximal increment of PRA after the infusion in both s-EH and N.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension]. 632 58


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