Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Fourteen mildly hydropenic normal volunteers were slowly tilted at a constant rate from the horizontal to the 85 degrees head-up position in order to study the interrelationship between plasma arginine vasopressin concentration, plasma renin activity and the change of plasma volume. 2. Nine subjects did not develop vaso-vagal symptoms and were studied for 45-60 min. Arginine vasopressin rose biphasically in all subjects: a small initial rise, which was seen at 3 min and persisted for 30 min, was followed by a striking rise between 30 and 45 min, when the fall of plasma volume had reached its maximum (17%). 3. Plasma renin activity reached a maximum at 30 min but fell by 45 min, as plasma concentration of arginine vasopressin rose. 4. Five subjects developed vaso-vagal symptoms 4-24 min after reaching 85 degrees when the study was terminated. A striking increase of arginine vasopressin concentration was seen within 4 min of syncope, but there was no change of plasma osmolality, cortisol concentration or renin activity.
Clin Sci Mol Med 1976 Sep
PMID:The response of arginine vasopressin and plasma renin to postural change in normal man, with observations on syncope. 96 56

1. The participation of neural mechanisms in mediating the renin release induced by reduction of renal perfusion pressure was explored in anaesthetized cats by comparing renin release from the two kidneys, one acutely denervated and the other intact. 2. Suprarenal aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and halved blood flow to both kidneys, but cause a greater release of renin from the innervated kidney than from the contralateral denervated one (increments of 72 +/- 17 and 29 +/-20 pmol/min respectively). 3. A study of the time-course of the response during aortic stenosis of 30 min duration showed early release of renin from the innervated kidney at a time (5 min) when little release occurred from the denervated one. In later samplings (15 and 30 min) the response of the innervated kidney levelled out at somewhat lower values, and that of the denervated organ progressively increased, but remained smaller than on the side with intact nerves. 4. There was no parallelism between renin release and renal vasomotor changes induced by aortic stenosis, as vasomotor changes were equal in the two kidneys and remained constant from beginning to end of stenosis. It is concluded that a significant part of the renin release induced by aortic stenosis is dependent on neural mechanisms: the neural differs from the non-neural component in being of more rapid onset and probably of shorter duration.
Clin Sci Mol Med 1976 Nov
PMID:Neural factors contributing to renin release during reduction in renal perfusion pressure and blood flow in cats. 99 43

1. Acute renal failure was produced in rats by intramuscular injection of glycerol. Subsequently, changes in the concentrations of renin and of angiotensin II in plasma and the renin content of the kidneys were followed. 2. at 4 and 8 h after glycerol administration, plasma renin and angiotensin II had increased two to three-fold; they remained elevated for 48 h and then returned towards normal. At 7 days, the values were still slightly raised. 3. At 4 and 8 h after glycerol injection, kidney renin had decreased but it had increased after 24 and 48 h. 4. Passive immunization with angiotensin II antibodies, given at the time of glycerol injection and 2 and 4 h afterwards, prevented the development of acute renal failure. When angiotensin II antiserum was administered later (8, 10 and 12 h after glycerol) it had no effect. 5. Stimulation of the renin-angiotensin system may be involved in the pathogenesis of the early phase of acute renal failure.
Clin Sci Mol Med Suppl 1975 Jun
PMID:The renin-angiotensin system in acute renal failure of rats. 105 77

1. In patients with mild or moderate essential hypertension, oral propranolol, given in incremental doses, produced a moderate but significant lowering of blood pressure which was correlated with the concentration of propranolol in plasma. 2. Propranolol also reduced plasma renin activity (PRA) in the supine posture, on standing and after intravenous frusemide. However, 'supine' and 'frusemide' PRA values were markedly reduced at a plasma concentration of propranolol that had little effect on blood pressure. 3. On administration of propranolol there was little correlation between blood pressure decrease and PRA suppression, and even less between pretreatment PRA values and hypotensive response. 4. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, suppression of PRA is not an important determinant of the hypotensive response to propranolol.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Hypotensive and renin-suppressing activities of propranolol in hypertensive patients. 105 79

1. The effect of propranolol on total and regional renal blood flow was measured in conscious rabbits after 6 days on normal or low sodium diets. 2. Propranolol inhibited the fall in total superficial cortical renal blood flow which occurred in response to the low sodium diet but did not influence renal blood flow in rabbits on a normal sodium diet. 3. Reduction and redistribution of renal blood flow in response to a low sodium diet appears to be mediated by a beta-receptor mechanism and may be a consequence of intrarenal release of renin.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Effects of beta-adrenergic receptor blockade on the renal vascular response to a low sodium diet in the rabbit. 105 84

1. The effect of diazoxide (17-3 micronmol min-1 g-1) and frusemide (0-12 micronmol min-1 g-1) on renin secretion was examined in the isolated perfused rat kidney. These substances are potential renal vasodilators with opposite effects on urine sodium excretion. 2. Both agents significantly increased renin secretion rate above control values. In the case of frusemide this was not altered by ureteric occlusion and presumed absence of urine flow. 3. Mean renal perfusion pressure decreased to the same extent with diazoxide and frusemide infusion as in the control experiments and no additional vasodilatory effect was observed on the basis of changes in flow rate of perfusate. 4. These observations identify an intrarenal site of action for diazoxide and frusemide on renin secretion. The apparent independence of this stimulatory action on renal vasodilation and urine flow suggests a direct effect on the renin-producing cell.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Stimulation of renin secretion by frusemide and diazoxide in the isolated rat kidney. 107 82

1. Reduction of renal perfusion pressure from 133 mmHg to 117 mmHg in control rats did not induce a significant change of kidney glomerular filtration rate (GFR) or nephron GFR determined in distal tubules. In contrast, nephron GFR measured in proximal tubular segments (NGFR-P) fell significantly. 2. Qualitatively the same response of filtration rate to changes of arterial blood pressure was found in the chronically clipped kidneys of Goldblatt hypertensive rats after acute removal of the clip. 3. In contrast, autoregulation of kidney GFR, NGFR-D and NGFR-P was abolished in the contralateral kidneys of Goldblatt hypertensive rats. 4. Microperfusion studies showed that tubuloglomerular feedback regulation of NGFR was present in the renin-rich ischaemic kidneys of Goldblatt rats after removal of the constricting clip, but greatly attenuated in the renin-depleted contralateral kidneys. 5. These data indicate that tubuloglomerular feedback participates in establishing renal autoregulation, possibly by mediation of the renin-angiotensin system.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Inter-relationship between autoregulation of glomerular filtration rate, tubuloglomerular feedback and juxtaglomerular renin activity in normotensive and hypertensive rats. 107 83

1. Sympathetic reflexes were activated by carotid occlusion in anaesthetized dogs in which changes in renal perfusion pressure were prevented. This produced a prompt and reversible increase in plasma renin activity. 2. Administration of clonidine decreased plasma renin activity, arterial pressure and heart rate and blocked the renin secretory and blood pressure responses to carotid occlusion. 3. These results support the hypothesis that the suppression of renin secretion by clonidine is a consequence of the decrease in sympathetic activity produced by this drug.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of carotid occlusion and clonidine on renin secretion in anaesthetized dogs. 107 84

1. The metabolic role of arterial angiotensin I-forming enzyme (i.e. renin activity) was studied in total homogenates and in subcellular fractions of the aorta of normotensive and hypertensive rats. 2. Angiotensin I-forming enzyme was measured in (a) uninephrectomized rats rendered hypertensive with D-aldosterone and sodium chloride (10 g/l drinking solution, (b) rats treated in the same manner but with the addition of spironolactone, and (c) control rats. 3. Hypertension developed in aldosterone-treated rats within 3-6 weeks and was associated with decreased plasma and renal renin values. Total aortic renin activity was up to sixfold higher in the hypertensive animals than in control animals and there was an increased ratio of supernatant to microsomal renin activity in the aorta. 4. In spironolactone-treated rats blood pressure and total aortic renin concentrations were comparable with those in the control rats. 5. The results support the hypothesis that renin generated at local vascular sites, which is independent of circulating renin levels, contributes to regulation of blood pressure.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of aldosterone and spironolactone on arterial renin in rats. 107 85

1. Infusion of angiotensin II antagonist failed to restore the blood pressure of short-term Goldblatt 2-kidney hypertensive rats to normal levels before and after sodium restriction. 2. The blood pressure of both normal and sodium-restricted Goldblatt 2 hypertensive rats remained elevated 6 h after bilateral nephrectomy. 3. The residual hypertension found during antagonist infusion and after bilateral nephrectomy is not maintained by the renin-angiotensin system or sodium retention.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The role of sodium retention in Goldblatt 2-kidney hypertension in the rat. 107 86


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