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)

We examined renal tubular function in six patients with sickle cell hemoglobin. All had normal inulin and para-aminohippurate clearances and impaired urinary concentrating and acidifying abilities. After intravenous potassium chloride administration, maximum excretion of potassium (U,V) was significantly lower in sickle cell patients than in control subjects, and the percentage of potassium load excreted in 5 h was markedly reduced. Urinary potassium excretion after sodium sulfate infusion was also markedly reduced in sickle cell patients compared to control subjects. After 40 mg of oral furosemide, U,V was also diminished in sickle cell patients. Plasma aldosterone response to ACTH and intravenous potassium was similar to that of control subjects. Plasma renin activity increased normally after volume contraction. We conclude that sickle cell patients have a defect in their ability to excrete an acute potassium load that cannot be attributed to abnormal renin or aldosterone secretion. Overall potassium homeostasis is maintained by extrarenal mechanisms during acute potassium loading.
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PMID:Impaired renal tubular potassium secretion in sickle cell disease. 3 41

The effect of metabolic acidosis on the renin-aldosterone system remains unclear. In the present study anesthetized mongrel dogs (n = 19) were infused at similar rates with 0.45% NaCl (controls), HCl or NH4Cl (2.5mEq/kg) for 1--3 h. The induced metabolic acidosis in the two experimental groups was not associated with increases in plasma renin activity. Plasma cortisol (as a marker for ACTH secretion) and serum potassium concentration increased in both HCl- and NH4Cl-treated animals. Plasma aldosterone increased after 30 min in the HCl group and 60 min in the NH4Cl group and did not change in controls. These findings demonstrate that metabolic acidosis induced by HCl or NH4Cl is associated with increased aldosterone production without concomitant changes in plasma renin activity.
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PMID:The effect of acute metabolic acidosis on plasma cortisol, renin activity and aldosterone. 3 26

Heparin and the heparinoid Ro 1-8307 inhibited the secretory rate of aldosterone in physiological or pathological aldosteronism to the level found in normal subjects on liberal sodium intake. In addition, these compounds inhibited corticosterone biosynthesis, although less markedly than that of aldosterone. Indications of interference with cortisol production have not been found. During drug treatment angiotensin, in doses of 5-10 ng/kg b.wt./min, did not stimulate aldosterone secretion. ACTH responsiveness of the adrenals--indicated by the fractional increases of both aldosterone and corticosterone secretory rates--remained unchanged. In two studies heparin had no consistent effect on plasma renin activity.
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PMID:Inhibition of adrenal function in man by heparin or heparinoid Ro 1-8307. 4 2

The effect of incremental infusions of isoleucine-5-angiotensin II on blood pressure and plasma aldosterone concentrations was studied in normal man before and after 66 hours of intravenous infusion of angiotensin II at 2 ng kg-1 min-1, sodium and potassium balance being kept roughly constant throughout. Plasma sodium and ACTH concentrations were unaltered, but plasma potassium and magnesium levels and basal plasma cortisol fell slightly after prolonged angiotensin administration. During the prolonged angiotensin infusion plasma renin activity was suppressed, and there was a sustained elevation of arterial pressure and plasma aldosterone concentration. Aldosterone excretion, while clearly increased, showed a regular circadian rhythm, with peak values in the early morning. The angiotensin II-pressor relationship was not significantly changed after the prolonged infusion of angiotensin II, while the angiotensin II-aldosterone dose-response curve was steeper than in the basal state but not identical with that of sodium depletion. No differences were observed in the pressor or aldosterone-stimulant effects of the isoleucine-5 and valine-5 forms of angiotensin II. A trophic effect of angiotensin II on the adrenal cortex may provide a partial explanation for the enhanced response of aldosterone to angiotensin II in sodium depleted man.
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PMID:Effect of prolonged low-dose angiotensin II infusion on the sensitivity of adrenal cortex in man. 16 8

In order to evaluate the control of the circadian rhythm of plasma aldosterone concentration in man, plasma aldosterone, cortisol, sodium and potassium concentrations, and plasma renin activity (PRA) were measured in samples obtained at 20-minute intervals from 0200 to 0800 in sodium repleted (180 mEq. per day of diet) and sodium depleted (22 mEq. per day of diet) normal subjects. During sodium replete studies, plasma aldosterone and cortisol concentrations were significantly correlated (p greater than 0.01) in all 4 subjects. Plasma aldosterone also correlated with PRA (p greather than 0.01) in 2 subjects and with potassium (p greater than 0.01) in one. Episodic increases in plasma aldosterone concentration were observed despite suppression of ACTH by dexamethasone treatment. Plasma aldosterone concentrations were significantly correlated with PRA (p greater than 0.05 and p greater than 0.01) in only 2 of 4 subjects under these conditions. Following sodium restriction, plasma aldosterone concentrations were not significantly correlated with plasma cortisol and only infrequently with either PRA or potassium. When dexamethasone was administered during the low sodium diet, correlations with PRA (p greater than 0.001) were seen in 2 of 3 subjects and with potassium (p greater than 0.01) in 1 of 3 subjects. There was no significant correlation between plasma aldosterone and sodium concentration during any of the studies. These results are compatible with the concept that the relative importance of PRA, ACTH, and potassium in inducing changes in aldosterone production during the early morning hours is partially dependent upon dietary sodium, but also varies between individuals studied during similar sodium diets. The episodic alterations of plasma aldosterone concentration continued after ACTH was suppressed by dexamethasone pretreatment. These changes, in the absence of a consistent significant correlation with PRA and sodium and potassium concentrations, further suggest that another factor(s) may be important in controlling aldosterone production in recumbent normal subjects.
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PMID:The effect of dexamethasone on the control of plasma aldosterone concentration in normal recumbent man. 16 19

Using a newly developed radioassay method, plasma 11-deoxycorticosterone (DOC) levels were studied in 6 human volunteers for diurnal variation and for response to ACTH, metyrapone, dexamethasone, and low or high dietary sodium. DOC reached its peak of 6.4 +/- 1.2 ng/100 ml at 8:00 AM, and its nadir of less than 1 ng/100 ml at midnight. Corresponding plasma cortisol values were 14.1 +/- 1.4 mug/100 ml and 5.9 +/- 1.3 mug/100 ml respectively. After intramuscular ACTH (Cortrosyn 0.25 mg), DOC rose to 28.7 +/- 1.8 ng/100 ml in 1 h. Dexamethasone treatment for 3 days reduced DOC to less than 1 ng/100 ml in all 6 subjects. Oral metyrapone for 24 h resulted in dramatically elevated DOC levels of 1568 +/- 183 ng/100 ml. High dietary sodium did not affect DOC levels which averaged 5.6 +/- 0.7 ng/100 ml. After 3 days of sodium restriction, DOC levels were unchanged at 4.8 +/- 0.5 ng/100 ml (P greater than 0.9) despite high plasma renin activity and elevated plasma and urinary aldosterone. Dexamethasone was then added, and the diet continued for a further 2 days. In contrast to the effect of dexamethasone during ad lib sodium intake, DOC was not suppressed but slightly elevated to 8.6 +/- 1.4 ng/100 ml (P = 0.01), whereas plasma aldosterone decreased from 32.9 +/- 1.5 to 22.1 +/- 2.1 ng/100 ml. Seven additional subjects underwent the same diet for 5 days without the addition of dexamethasone. There was no change in their DOC values. It is concluded that the zona fasciculata is the main source of DOC, but in the presence of dexamethasone a contribution from the zona glomerulosa during sodium depletion is uncovered.
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PMID:The contribution of the zona fasciculata and glomerulosa to plasma 11-deoxycorticosterone levels in man. 16 27

In order to investigate the role of renin secretion and of ACTH on the circadian rhythm of plasma aldosterone (PA), plasma renin activity (PRA), plasma cortisol (PC) and PA were determined at short-time intervals in 10 normal supine men. Six subjects were studied under a normal sodium intake and 4 under sodium restriction. In 4 subjects the secretion of ACTH was suppressed by dexamethasone. Under normal sodium intake changes in PA seemed to be more in parallel with changes in PC than by those in PRA as indicated by a higher significant correlation between PA and PC than between PA and PRA in 3 of the 4 subjects. In 1 subject no correlation was observed between PA and PC despite visual synchronism between the plasma concentrations of both hormones. Under dexamethasone medication fluctuations in PA were followed by those in PRA while PC was less than 2 mug/100 ml. In the sodium restricted state, changes in PA were closely paralleled and significantly correlated to PRA while no correlation was seen between PA and PC. Under dexamethasone medication the significant correlation between PA and PRA persisted. Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Under normal sodium intake ACTH seems to be the dominant factor controlling PA, whereas under sodium restriction changes in PA are mediated through the renin angiotensin system. When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake.
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PMID:Diurnal variations of plasma aldosterone in supine man: relationship to plasma renin activity and plasma cortisol. 16 14

In the present study a comparison was made on the role of the renin-aldosterone system in rats with various forms of experimental hypertension (pinealectomy-induced, renal and spontaneous). The plasma sodium and potassium concentrations as well as renin activity were measured. The in vitro production of aldosterone by quartered adrenal glands of these rats was also determined. 5 weeks after the operations the blood pressure of the pinealectomized and renal operated rats was significantly increased. The plasma sodium concentration did not differ in various groups, but that of potassium was decreased in the renal hypertensive animals. The plasma renin activity of the pinealectomized rats was elevated while in other forms of hypertension it was at the control level. The basal aldosterone production by the adrenal quarters was equal in all the groups. ACTH, dibutyryl cyclic adenosine-3',5'-monophosphate (DBA) and 5HT stimulated the aldosterone production. The responses to ACTH and DBA were greater in the adrenals of renal hypertensive rats than in the other forms of hypertension or in the controls. We suggest that the renin-aldosterone system is of importance in the maintenance of renal hypertension, while in pinealectomy-induced hypertension elevated plasma renin activity reflects an increased sympathetic activity which probably is the main cause of hypertension in these animals.
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PMID:Plasma renin activity and in vitro synthesis of aldosterone by the adrenal glands of rats with spontaneous, renal, or pinealectomy-induced hypertension. 16 35

The temporal changes of aldosterone concentration and renin activity in plasma under the influence of stimulating and inhibiting factors were tested in two patients with Bartter's syndrome. There was a normal response to potassium and sodium administration, spironolactone, angiotensin II, ACTH and dexamethasone. Changes in plasma-aldosterone concentration, as measured at frequent intervals during angiotensin II infusion, suggest differential regulation of aldosterone synthesis by angiotensin II. In one patient the symptoms improved with administration of glucocorticoid derivatives.
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PMID:[Plasma-aldosterone and renin activity in Bartter's syndrome (author's transl)]. 17 Nov 32

The role of ACTH in the control of aldosterone secretion has been investigated in volunteers under a normal sodium diet. Endogenous ACTH suppression by dexamethasone (DXM) does not alter the plasma aldosterone (PA) response to 20 mg furosemide since identical PA increases are observed in control subjects and in subjects with DXM suppressed endogenous ACTH. The sodium depletion induced by furosemide during continuous ACTH infusion increases plasma renin activity but does not change PA.
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PMID:[Proceedings: Role of endogenous and exogenous ACTH on aldosterone secretion (author's transl)]. 17 3


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