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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Blood pressure, plasma renin activity, plasma aldosterone, urinary noradrenaline during sleep (UNA-S) and several estimates of sodium intake were determined in 379 normotensive subjects (age 13--70) to investigate the relationship of these variables to blood pressure. 2. Blood pressure was correlated with age, weight, plasma renin activity UNA-S, and estimates of sodium intake. There variables were frequently intercorrelated. 3. Multiple-correlation analysis revealed that after removal of the effects of age, blood pressure was related to weight, plasma renin activity, UNA-S and estimates of sodium intake. 4. However, multiple-regression analysis failed to demonstrate an effect of plasma renin activity, UNA-S, or estimates of sodium intake on blood pressure when the effects of age, weight, race and sex were removed. 5. Careful matching of subjects by age, weight, race and sex in studies of blood pressure and biochemical factors in normal subjects is crucial to proper interpretation of such data.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Biochemical correlates of the increase in blood pressure with age. 28 91

1. In 20 subjects with uncomplicated essential hypertension, 10 of whom were on propranolol treatment, several blood samples were drawn simultaneously from the renal artery and vein after angiographic studies. In these samples we determined concentrations of noradrenaline, active renin, aldosterone and cortisol. 2. Renal blood flow was measured in all patients by Hippuran-clearance and xenon-washout. 3. Despite marked variations in the arteriovenous difference of noradrenaline, it was apparent in both groups that the kidney is able to release noradrenaline. 4. In the propranolol-treated group noradrenaline secretion with untreated hypertensive patients.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Noradrenaline secretion by the human kidney. 28 5

1. In order to demonstrate whether modification of aldosterone secretion is mediated by parallel changes of K+ in the adrenal zona glomerulosa, the total (intracellular+extracellular) Na+ and K+ content of the rat adrenal cortex was determined with the electron microprobe. 2. Groups of rats were submitted to one of the following dietary regimens: standard, low Na+, high K+ or high Na+. 3. Distribution of Na+ and K+ across the zona glomerulosa and zona fasciculata was compared. Standards of known electrolyte concentration were also analysed. 4. The [Na+] was found to be greater in the zona glomerulosa than in the zona fasciculata but K+ was distributed evenly in both zones. This was independent of dietary regimen. 5. Aldosterone production, assessed by plasma aldosterone concentrations, could not be correlated with zona glomerulosa K+ content.
Clin Sci Mol Med 1977 Nov
PMID:Detection of Na+ and K+ in the rat adrenal cortex with the electron microprobe. 58 27

1. The effect of intravenous loading with 500 ml of sodium chloride solution (50 g/l) on plasma renin concentration, plasma aldosterone concentration, urinary sodium excretion and mean blood pressure was studied in 15 young patients with mild essential hypertension and 10 healthy normotensive control subjects. 2. Plasma renin concentration and plasma aldosterone concentration were suppressed to the same degree during loading in both the hypertensive and normotensive groups. Urinary sodium excretion was significantly higher in the hypertensive patients than in the normotensive subjects. Mean blood pressure increased slightly in both groups. 3. Plasma renin concentration and plasma aldosterone concentration were significantly correlated in both groups before sodium loading. The increase in urinary sodium excretion was significantly correlated to the suppression of plasma aldosterone concentration in the hypertensive, but not in the normotensive, group. No correlation was found between changes in urinary sodium excretion and changes in plasma renin concentration or mean blood pressure. 4. The results indicate that the suppressibility of the renin-aldosterone system by hyperosmotic sodium chloride solution is normal in young patients with mild essential hypertension. It is suggested that the changes in plasma aldosterone concentration induced by sodium loading might be involved in the regulation of exaggerated natriuresis in essential hypertension.
Clin Sci Mol Med 1977 Dec
PMID:The renin-aldosterone system in exaggerated natriuresis of essential hypertension. 58 41

1. Serial measurements of plasma renin activity (PRA), plasma aldosterone concentration (PA) and blood pressure were performed overnight in patients with borderline (group 1) and sustained essential hypertension (group 2) before and after acute and chronic administration of either propranolol or pindolol. 2. Group 1 patients exhibited a typical rhythm of recumbent PRA with low values before midnight and large increases early in the morning. 3. In contrast, no rhythm and very low PRA values were observed in patients of group 2. Blood pressure was higher in group 2 than in group 1. There was a significant correlation between the hyporeninaemic and hypotensive effect of either acute (r = 0-79) or chronic (r = 0.4) beta-receptor blockade. 4. In group 1, after beta-receptor blockade the day-night profile of renin was similar to that observed in group 2 before treatment. Thus, in this latter subgroup, low-renin profiles might reflect reduced beta-adrenoreceptor activity. 5. Plasma aldosterone was lower in group 2 but appeared to be inappropriately high relative to renin. 6. The data suggest that in hypertensive patients classified according to their blood pressure and recumbent PRA profiles a significant relationship exists between changes in PRA and arterial pressure. Thus patients with high PRA respond better to treatment than patients with low renin. We conclude that in the patients studied sympathetic nervous system activity mainly determined renin values as well as anti-hypertensive effectiveness of the beta-blocking drugs.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Differential effects of acute and chronic beta-adrenoreceptor blockade on blood pressure and the renin-angiotensin-aldosterone system in essential hypertension. 79 64

1. The changes in plasma volume, haemodynamic variables, plasma renin activity and plasma aldosterone were studied in forty-one hypertensive patients after administration of adrenergic-blocking agents. Four drugs were used: alpha-methyldopa (fourteen patients), guanethidine (ten patients), clonidine (nine patients) and reserpine (eight patients). Drugs were administered orally during 7 days' hospitalization on a normal sodium diet (110 mmol/day). 2. The four drugs had similar effects: a significant decrease in blood pressure, a significant increase in plasma volume and no change in stroke volume. 3. With alpha-methyldopa and guanethidine, heart rate, plasma renin activity and plasma aldosterone were unchanged. 4. With reserpine and clonidine, heart rate and plasma renin activity were significantly decreased, whereas plasma aldosterone did not change significantly. 5. This study suggests that the decrease in plasma renin activity was related to the lowering of the heart rate rather than to sodium retention and that adrenergic-blocking agents can impair the normal relationship between stroke index and plasma volume, between plasma volume and plasma renin activity, and between plasma renin activity and plasma aldosterone.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Anti-hypertensive adrenergic-blocking agents: effects on sodium balance, the renin-angiotensin system and haemodynamics. 80 49

1. Adrenocorticotrophic hormone-suppressed, bilaterally nephrectomized male mongrel dogs (n = 12) were infused with Sar1-angiotensin II and Asp1-angiotensin II, the naturally occurring octapeptide. 2. Sar1-angiotensin II was found to be almost twice as potent as Asp1-angiotensin II in elevating blood pressure but its aldosterone-stimulating activity was not higher than that of the naturally occurring peptide. 3. A specific competitive antagonist of angiotensin II, Sar1-Ile8-angiotensin II, blocked the pressor but not the aldosterone-stimulating activity of Sar1-angiotensin II. 4. These results suggest functional differences in receptors for angiotensin II in vascular smooth muscle and in adrenal cortex.
Clin Sci Mol Med 1976 Jul
PMID:Differential effects of Asp-angiotensin II and Sar-angiotensin II on vascular and adrenal receptors in the dog. 93 65

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.
Clin Sci Mol Med 1976 Jul
PMID:Effect of sotalol on haemodynamics and renin-angiotensin-aldosterone system in hypertensive patients. 93 70

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. The effect of infusions of equimolar doses of angiotensin II (AII) and of Des -angiotensin II (heptapeptide) on plasma renin activity, blood pressure and plasma aldosterone were compared in normal anaesthetized dexamethasone-suppressed dogs. 2. Plasma renin activity was equally suppressed by both compounds. The increase in blood pressure induced by the heptapeptide averaged 43-62% of the increase during AII infusions. No significant differences in aldosterone increase were observed between AII and the heptapeptide. Plasma aldosterone, however, dropped significantly faster in heptapeptide-treated dogs after the end of the infusions. 3. Sar -Ala -angiotensin II (saralasin, 400 pmol min-1 kg-1) suppressed plasma aldosterone that was stimulated by heptapeptide (20 pmol min-1 kg-1) completely. The same angiotensin antagonist had only a moderate effect on plasma aldosterone stimulated by AII. After stopping the antagonist infusion, plasma aldosterone rose significantly higher in dogs infused with AII than in those receiving the heptapeptide. 4. The results demonstrate differences between the effects of AII and the heptapeptide both on blood pressure and on plasma aldosterone. They do not support the hypothesis that the heptapeptide may be the main mediator of aldosterone secretion.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Studies on the effect of angiotensin II and of Des -angiotensin II on blood pressure, plasma renin activity and plasma aldosterone in the dog. 107 93


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