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)

CaCl2 suppresses the plasma renin activity (PRA) response to Na+ deprivation in the rat. The purpose of the present study is:1) to determine if the effect of Ca2+ on PRA is modified by the anion delivered with Ca2+, and 2) to evaluate the effect of Ca2+ loading on aldosterone production. PRA and in vitro aldosterone production by adrenal quarters were measured after a 7-day balance study. On a low Na+ diet, PRA of animals drinking 1% CaCl2 (13.1 ng/ml per h +/- 1.3 SE), but not of animals drinking 1% calcium gluconate, was suppressed (P less than 0.05) compared to that of water-drinking controls (20.9 ng/ml per h +/- 2.1 SE). Aldosterone production of calcium gluconate and CaCl2-loaded animals was greater than that of controls (P less than 0.01). K+ balance of CaCl2 and calcium gluconate-drinking animals was more positive than that of controls (P less than 0.05). In conclusion, inhibition of PRA by CaCl2 but not by calcium gluconate indicates that the effect of Ca2+ on PRA is modified by the accompanying anion. Both CaCl2 and calcium gluconate stimulate aldosterone production, independent of changes in PRA, possibly due to an effect of Ca2+ on K+ balance.
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PMID:Effects of calcium on renin and aldosterone in the rat. 1 57

1. A denervated 'auto-transplanted' dog's kidney preparation was developed to study renin release into renal plasma and lymph. The function of the 'transplant' was compared with that of its partner. In the 'basal' state it had a similar rate of plasma and urine flow, Na, Ca, Mg and Cl excretion but a lower rate of glomerular filtration and K excretion and a lower urinary osmolality. In the 'basal' state the 'transplant' did not release renin into plasma, but invariably released it into lymph. 2. Infusions of MgCl2 solutions into the renal artery which raised the renal plasma Mg concentration (PMg) by 0.1-2 m-mole.1.-1 provoked a concentration-related increase in renin release into plasma. This was due to a rise in the veno-arterial renin difference and in the renal plasma flow rate. Blood pressure and Na excretion were unaltered. 3. In other experiments, an increase in PMg of 1.5-2.5 m-mole.1.-1 was also found to increase renin release into lymph. 4. When the plasma Ca concentration was doubled by infusion of CaCl2 into one renal artery, an increase in PMg of 1.5-2.5 m-mole.1.-1 no longer increased renin release into plasma or lymph. 5. When the plasma NaCl concentration was raised by 8-15 m-mole.1.-1 by infusion of hypertonic saline into the renal artery, MgCl2 infusion failed to increase renin release until PMg was raised by more than 3 m-mole.1-1. 6. The results demonstrate that hypermagnesaemia stimulates renal renin release by a mechanism that is independent of the renal nerves, or of any changes in blood pressure or sodium excretion, but which is antagonized by concurrent hypercalcaemia or hypersalaemia. The possibility is discussed that Mg is reabsorbed from the tubular into the interstitial fluid where it antagonizes the action(s) of Ca on renin release from the juxtaglomerular cells.
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PMID:The effect of increasing the plasma magnesium concentration on renin release from the dog's kidney: interactions with calcium and sodium. 36 8

The present study was undertaken to isolate and investigate some physicochemical properties of renin granules from the rat kidney cortex. Two preparations of subcellular organelles were used: a primary-granule fraction, which allowed the properties of lysosomes to be compared simultaneously with those of renin granules, and a semi-purified preparation of the latter. The specific activity of renin in the primary-granule preparations was about 4-fold higher than in the original homogenate; that of the semi-purified renin-granule preparation was about 18-fold higher than in the homogenate, and consisted mainly of electron-dense granules but some mitochondria were also observed. Renin and acid phosphatase release from the primary-granule preparation was increased by lowering osmolality, by a low-molecular-weight solute (glucose) and by Triton X-100 or digitonin. Enzyme release was decreased by lowering the incubation temperature (4 degrees C) or the presence of CaCl2. Renin release from the partially purified granule preparation was not affected by cyclic AMP, cyclic GMP and ATP.
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PMID:Studies on the isolation and properties of renin granules from the rat kidney cortex. 50 86

We have previously reported that infusion of CaCl2 into the renal artery of the dog inhibits renin release. To evaluate the possible importance of the anion delivered with calcium, similar experiments were performed in 10 dogs with equivalent amounts of calcium gluconate (0.3 mg. of Ca++ per kilogram of body weight per minute). The experiment consisted of three successive 15 minute control periods, followed by three 15 minute calcium gluconate infusion periods and two 15 minute recovery periods. During calcium gluconate infusion, mean serum Ca++, and ECa++, ENa+, and EFNa+ from the infuses kidney increased (p less than 0.005). Systolic blood pressure (142 mm. Hg +/- 8S.E.), renal blood flow (137 ml. per minute +/- 11 S.E.), creatinine clearance, and aldosterone excretion (12.0 ng. per 15 minute +/- 1.5 S.E.) did not change (p less than 0.3). Renal venous PRA (28.4 ng. per millileter per hour +/- 7.5 S.E.) decreased (p less than 0.014). The per cent decrease of PRA correlated (r = -0.70) with the per cent increase EFNa+ (p less than 0.001). Calcium gluconate had a lesser (p less than 0.01) inhibitory effect on renin than CaCl2, despite greater excretion of Ca++ and Na++ during calcium gluconate infusion. Taken together, the results indicate that Ca++ inhibits renin release, although the extent of the inhibition is modified by the anion accompanying Ca++. The effect of Ca++ on renin may be mediated by NaCl transport across the macula densa.
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PMID:Effect of calcium gluconate infusion on renin in the dog. 83 Jul 78

We studied the effects of intrarenal calcium infusion on renin secretion in sodium-depleted dogs in an attempt to elucidate the major site of calcium-induced inhibition of renin release. Both calcium chloride and calcium gluconate reduced renal blood flow and renin secretion while renal perfusion pressure was unchanged. These data indicate that calcium inhibition of renin secretion did not occur primarily at the renal vascular receptor; decreased renal blood flow is usually associated with increased renin secretion. Calcium chloride infusion increased urinary chloride excretion without affecting sodium excretion, and calcium gluconate failed to increase either sodium or chloride excretion. Also, the filtered loads of sodium and chloride were unchanged during the calcium infusions. These results give no indication that calcium inhibited renin secretion by increasing the sodium or chloride load at the macula densa. The effects of intrarenal calcium infusion on renin release were also assessed in dogs with a nonfiltering kidney in which renal tubular mechanisms could not influence renin secretion. The observation that calcium still suppressed renin release in these dogs provides additional evidence that the the major effect of calcium involved nontubular mechanisms. Thus, it appears likely that calcium acted directly on the juxtaglomerular cells to inhibit renin secretion.
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PMID:Intrarenal site of action of calcium on renin secretion in dogs. 100 Jul 79

The effects of calcium and deoxycorticosterone (DOC) on blood pressure, plasma renin activity (PRA), urinary sodium excretion and aortic responses were studied in spontaneously hypertensive rats (SHR). The animals (age 9 weeks) were divided into four treatment groups: control, calcium, DOC and DOC+calcium (n = 12 and the mean systolic blood pressure 174-177 mmHg in each). Calcium was given as 1.5% CaCl2 in drinking fluid, and DOC trimethylacetate by weekly injections (25 mg/kg s.c.). During the 4-week study systolic blood pressure rose in all groups, but the increase was attenuated by calcium (final levels: control 201 +/- 3, calcium 186 +/- 3, DOC 206 +/- 2, DOC + calcium 203 +/- 2 mmHg, mean +/- SE). PRA was reduced in both groups receiving DOC, but it was not affected by calcium. Calcium supplementation increased urinary excretion of sodium in DOC-treated animals. DOC enhanced the in vitro contractility of helically cut aortic strips to noradrenaline, and decreased the relaxation of the strips to nitroprusside and nifedipine. The results indicate that calcium supplementation attenuates the development of hypertension in SHR, and that this attenuation is not mediated by the renin-angiotensin system. DOC abolished this lowering effect of calcium on blood pressure possibly by its action on vascular smooth muscle, resulting in increased vascular contractility and impaired relaxation.
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PMID:Effects of calcium and deoxycorticosterone on blood pressure, plasma renin activity and vascular reactivity in spontaneously hypertensive rats. 225 85

The effects of oral calcium loading on blood pressure (BP) of DOCA (deoxycorticosterone acetate)-salt hypertensive rats (D-S rats) were investigated. Calcium loading was performed by adding 1% CaCl2 (calcium chloride) to the drinking water. Calcium loading attenuated the development of high BP in D-S rats, and at the end of a two week experiment, BP was 141 +/- 3 (calcium treated) vs. 174 +/- 7 mmHg (non-calcium treated) (p less than 0.01). However, calcium loading did not cause any changes in BP in normotensive rats. Further, in established D-S rats [after four weeks of DOCA and 1% NaCl (sodium chloride) treatment], calcium loading for 4 weeks also reduced BP [144 +/- 6 (calcium treated) vs. 181 +/- 4 mmHg (non-calcium treated), p less than 0.01, at the end of experiment]. With calcium treatment, there were no significant changes in sodium-water balance, plasma levels of epinephrine and norepinephrine, plasma renin activity, plasma aldosterone concentration and serum electrolytes both in developing and established D-S rats. The depressor mechanism of calcium loading was studied by observing vascular responsiveness to norepinephrine both in whole body and in hind limb preparations. Vascular reactivity in both developing and established D-S rats was significantly attenuated by calcium treatment. These results suggest that the antihypertensive effects of calcium treatment in D-S rats are mainly caused by attenuation of vascular reactivity.
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PMID:Effects of calcium loading in DOCA-salt hypertensive rats. 332 56

1. In response to furosemide-induced sodium depletion pigeons showed a robust salt appetite. Following the 1st depletion they started to ingest 3% NaCl after a latency of 373 +/- 69 s and in 24 h they took 21.16 +/- 3.07 ml of this solution (vs. a daily mean intake of 1-2 ml prior to the depletion). 2. The appetite was selective as shown by the fact that when, after depletion, 0.34 M-CaCl2 was offered (which is equiosmotic to 3% NaCl) pigeons took just a trivial amount of it. 3. Analysis of sodium losses following the natriuretic treatment revealed that pigeons respond to sodium depletion with an excessive overconsumption of NaCl solution. In the 2 h after access to salt they took about 3 times the amount of sodium lost. 4. Repeated sodium depletions sharply reduced the latency to the ingestion of salt and produced larger intakes. However, the overall amount of salt taken in 24 h after the later depletions was very similar and statistically indistinguishable from that taken following the 1st depletion. 5. Subchronic deoxycorticosterone acetate treatment (2 mg pigeon-1 day-1 I.M.) increased daily 3% NaCl intake, but large variability was observed in the response. 4 mg pigeon-1 day-1 evoked a reliable 3% NaCl intake which was particularly marked from the 5th day of the treatment. 6. Pulse intracerebroventricular (I.C.V.) injection of purified hog renin evoked water intake within about 1 min of injection, followed (about 6 h later) by increased salt intake. In the 24 h after renin injection pigeons took 16.58 +/- 2.89 ml of 3% NaCl. On the 2nd day following injection salt intake was still higher than in controls. 7. In conclusion, our results show that pigeons respond to sodium depletion with a robust salt appetite. Moreover, salt appetite can be evoked by deoxycorticosterone acetate as well as by renin. These findings suggest that in the pigeon salt appetite may be an endocrine-induced behaviour controlled by mineralocorticoids and by the renin-angiotensin system.
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PMID:Salt appetite in the pigeon in response to pharmacological treatments. 332 83

It has been shown previously that ouabain, vanadate, angiotensin II and 0 and 60 mM KCl media have Ca-dependent inhibitory effects on renin secretory rates of rat renal cortical slices. In the present experiments, replacing extracellular CaCl2 with SrCl2 did not impair the inhibitory effects on renin secretion in this preparation. Moreover, methoxyverapamil antagonized the inhibitory effect of K-depolarization. The inhibitory effects and methoxyverapamil-induced antagonism of the inhibitory effect of K-depolarization, suggest that increased intracellular Sr++ can lead to inhibition of renin secretion, perhaps directly or perhaps by causing the release or mobilization of Ca++ from intracellular sites of binding or sequestration. These results add to the growing evidence that Ca++ plays an inhibitory second messenger role in the renin secretory process.
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PMID:Extracellular strontium substitutes for calcium in in vitro renin secretion. 351 Dec 20

The effects of dietary chloride restriction - alone or combined with sodium and potassium restriction - on aldosterone biosynthesis and the renin-angiotensin system were studied in rats. Treatment with a chloride-deficient diet led to a temporary decrease in the capsular adrenal conversions of corticosterone to 18-hydroxycorticosterone and aldosterone (manifest after 2 weeks but not longer apparent after 3 weeks), which was accompanied by a progressive rise in plasma renin activity and a moderate fall in plasma potassium. Combined restriction of sodium, potassium and chloride elicited a decreased activity of the enzyme(s) involved in late steps in aldosterone biosynthesis, an elevation of plasma renin activity to excessively high levels and a substantial hypokalaemia. Chloride repletion of these rats by the addition of NH4Cl or CaCl2 to their drinking fluid stimulated aldosterone biosynthesis while lowering plasma renin activity and raising plasma potassium. According to these observations, dietary chloride deficiency is another example of an experimental situation in which a high activity of the renin-angiotensin system contrasts with an unchanged or suppressed aldosterone biosynthesis. Most likely, this divergence is at least partly due to hypokalaemia which is induced during long-term chloride deficiency by a yet unknown mechanism.
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PMID:Divergent effects of dietary chloride restriction on aldosterone biosynthesis and the renin-angiotensin system in rats. 352 Nov 82


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