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)

The renal parenchyma of 5 crub-eating monkeys (Macaca irus) was wrapped by cellophane, and plasma renin activity, blood pressure and vascular permeability of ocular ground were measured in comparison with 5 unoperated control monkeys. The results demonstrated that increases of systolic arterial pressure, plasma renin activity, and permeability of the retinal vessels were found in 4 operated monkeys. There was no such abnormal finding in the unoperated control monkeys. Generally there was a rough parallelism among levels of plasma renin activity and systolic blood pressure, an increase of permeability of retinal vessels and fibrinoid angionecrosis and/or necrotizing angitis similar to polyarteritis nodosa.
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PMID:Perinephritis hypertension in monkeys. I. An increase of plasma renin activity associated with increased permeability of retinal vessels and angionecrosis. 0 7

Propranolol administration in the hypoxic model of acute renal failure (ARF) in rats has reduced plasma renin activity (PRA) and uraemia as compared to untreated controls. P113 has no effect on uraemia but increased PRA in ARF. A combination of both drugs is no more effective in reducing uraemia than propranolol alone. These results support the view that beta-adrenergic blockade by propranolol reduces the severity of ARF by preventing the post-hypoxic release of renin.
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PMID:beta-Adrenergic blockade reduces the severity of acute renal failure in rats. 0 58

The effects of two new beta blockers on renal function have been studied. There were significant decreases in urine flow, urea clearance, sodium and chloride excretion rates after acute administration. Fractional excretion of sodium (FeNa) fell significantly but did not continue to fall during chronic administration. Blood pressure and plasma renin activity decreased significantly after two months' therapy. These findings suggest that beta blockers in patients with unstable cardiovascular function increase the need for concomitant diuretic therapy.
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PMID:Acute renal effects of new beta-adrenergic receptor site blocking agents on renal function. 0 59

The effects of metoprolol, a selective beta adrenergic receptor antagonist, on blood pressure, beta receptor blockade (antagoinst of isoproterenol and exercise tachycardia), and plasma renin activity (PRA) have been compared with those of placebo in 16 patients with essential hypertension. The dose of metroprolol was 25 mg three times daily for 1 wk and thereafter 100 mg three times daily for 5 wk. The mean decrease in blood pressure during treatment with metoprolol was 24 +/- 3.8 (SEM)/10 +/- 2.1 mm Hg in the lying position and 23 +/- 4.4/9 +/- 3.1 mm Hg after 1 min in the standing position. At a dose of 2.9 to 5.4 mg/kg, steady-state plasma concentrations of metoprolol varied 17-fold (from 20 to 341 ng/ml) between patients and correlated with the interindividual variability in isoproterenol antagonism (r = 0.58, p less than 0.05) and decrease in exercise tachycardia (r = 0.65, p less than 0.01). By contrast, neither of these variables correlated with the dose of metoprolol in mg/kg. Metoprolol decreased PRA by 67 +/- 1.9 and 71 +/- 1.2% in the lying and standing positions, respectively. The decrease in the mean arterial blood pressure in the lying position was significantly correlated to the PRA during the placebo period (r = 0.61, p less than 0.05) but not to the plasma steady-state levels of metoprolol, the degree of beta receptor blockade, and the decrease in PRA.
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PMID:Plasma levels and effects of metoprolol on blood pressure, adrenergic beta receptor blockade, and plasma renin activity in essential hypertension. 0 73

A double-blind placebo crossover trail (2 periods, each of 6 wk) was carried out in 12 patients. In the first period the patients were randomly allocated to either their individual established dose of prazosin or to the same number of placebo tablets; treatment was reversed after 6 wk. Blood pressure was higher by 17/8 mm Hgin the lying posture and by 24/14 mm Hg in the standing posture during placebo than during prazosin treatment. Standing pulse rate and body weight were higher and plasma renin activity lower during prazosin treatment. Postural hypotension occurring 1 to 2 hr after the first few doses was noted in one third of the patients when they resumed prazosin treatment after the placebo course.
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PMID:Effects of prazosin in patients with hypertension. 0 74

Basing on the literature data and their own observations of patients with chronic hemodialysis the authors have analysed the pathogenesis, course, hemodynamic shifts and possibilities of purposeful treatment in terminal uremia. Besides two variants of the hypertension course (controlled and noncontrolled), a third type has been revealed--hypertension difficult to control, in the pathogenesis of which, as well as in the noncontrolled variant, an important role is played by the activization of the renin-angiotensin system. Hemodynamic mechanizms of an abrupt change in the arterial pressure (acute hypotension and hypertensive crisis) in the process of hemodialysis are analysed.
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PMID:[Arterial hypertension and chronic hemodialysis]. 0

An isolated blood perfused kidney preparation was used to study the influence of intrarenal adrenergic receptors on renal hemodynamics, renal function, and the renin-angiotensin system. Beta adrenergic blockade with propranolol resulted in a reduction of fractional sodium excretion, and alpha blockade with phentolamine had no effect on sodium excretion despite significant increases in cortical flow and glomerular filtration rate. The changes in sodium excretion after beta blockade were not felt to be due to a direct tubular effect but rather were secondary to preferential perfusion of nephrons in the juxtamedullary cortex, which is known to have higher sodium reabsorptive capacity. These changes appeared to be direct effects of adrenergic blockade on the renal vasculature and were independent of any effects on renin secretion.
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PMID:Adrenergic blockade and renal hemodynamics. 0 45

I.v administration of propranolol (0.2 mg/kg and 1.0 mg/kg) to pentobarbital-anesthetized dogs produced blockade of cardiac beta-receptors and a significant decrease in heart rate. However, only the higher dose of propranolol demonstrated a significant hypotensive effect. Furthermore, this hypotensive action of propranolol was not associated with either adrenergic neruron blockade or changes in plasma renin activity. These results indicate that the initial hypotensive action of propranolol in mongrel dogs is not due to the blockade of beta-receptors, alterations in peripheral sympathetic nervous transmission or plasma renin activity. On the other hand, the action that propranolol is reported to have within the central system may play an important role in accounting for the acute blood pressure lowering action of the compound in mongrel dogs.
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PMID:Effect of propranolol of vascular responses to sympathetic nerve stimulation and plasma renin activity in mongrel dogs. 0 18

Studies in 55 patients with benign essential hypertension showed that the beta-blockers bufuralol (22 patients) and propranolol (33 patients) at a dose ratio of 1:4, possess comparable antihypertensive efficacy despite different properties regarding intrinsic sympathomimetic activity. Beta-blocker-monotherapy normalized blood pressure ( less than 140/90 mm Hg) in one fourth of the patients. Body weight and plasma and blood volumes remained unchanged during beta-blockade of four to six weeks duration, the mean plasma potassium was slightly increased. The inhibition of plasma renin activity (PRA) was more pronounced with propranolol (-69%) than with bufuralol (-47%). Wirth both beta-blockers decreases in blood pressure correlated inversely with pre-treatment PRA (p less than 0.05). Propranolol-induced changes in blood pressure correlated also with associated changes in PRA (p less than 0.005); in contrast, no such relationship was observed with bufuralol. The blood pressure effects of bufuralol, however, correlated significantly with changes in urinary noradrenaline excretion (r=0.41; p less than 0.05). Patient sub-groups with low, normal or high pre-treatment PRA in the average showed a comparable pattern of pre-treatment noradrenaline excretion and patients with normal renin levels exreted more adrenaline than those with low renin levels (p less than 0.001). These data are consistent with the concept that in untreated essential hypertension PRA may be an index of adrenergic activiity, the latter representing an important determinant of blood pressure response to beta-blockade. The blood pressure lowering effects of bufuralol in benign essential hypertension seem to be independent of renin and may be related, at least partly, to diminished free peripheral noradrenaline levels.
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PMID:[Interrelations between blood pressure, blood volume, plasma renin and urinary catecholamines during beta-blockade in essential hypertension (author's transl)]. 0 63

We previously reported that alpha- but not beta-adrenergic agonists stimulate renin release from mouse submaxillary glands in vivo. The present studies were undertaken to determine if these in vivo effects were due to a direct action on the submaxillary glands and to find out if cyclic AMP (cAMP) might be involved in submaxillary renin release. Pooled mouse submaxillary gland slices were incubated in Krebs-Ringer bicarbonate medium following a preincubation period, and renin release was measured by a radioimmunoassay for the direct measurement of submaxillary gland renin. Tissue cAMP levels were also measured. Addition of the alpha-adrenergic agonists, phenylephrine or norepinephrine, significantly increased renin release (P less than 0.01 vs. control) while decreasing tissue cAMP levels (P less than 0.01 vs. control). In contrast, addition of the beta-adrenergic agonist isoproterenol markedly increased cAMP levels (P less than 0.01 vs. control) and decreased renin release (P less than 0.05 vs. control). Pretreatment of the slices with the alpha-blocker phenoxy genzamine inhibited the effect of phenylephrine. These results indicate that alpha-adrenergic agonists cause renin release from submaxillary glands which is accompanied by a fall in tissue cAMP levels. This is in contrast to renin release from the kidney which is stimulated by beta-adrenergic agonists.
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PMID:Sympathetic nervous system and renin release from submaxillary glands in vitro. 0 95


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