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)

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 study the control system of plasma aldosterone in human, we examined the effects of low salt plus upright posture, angiotensin II, ACTH and potassium upon plasma renin activity, aldosterone and cortisol in five subjects who were supposed to be normal. All of the procedures, low salt diet with below 3 g of salt and 2 hr-upright posture, 0.25 mg of Cortrosyn, angiotensin infusion to increase 20mmHG of diastolic pressure for an hour, and 30 mEq of potassium infusion stimulated plasma aldosterone significantly. Furthermore, in each subject the degrees of response to each of these stimulations were almost same. In an old woman aged 68, responses to all of stimulations were significantly lower than those in other subjects. Plasma cortisol was significantly stimulated by ACTH, but slightly reduced by potassium infusion. From these results, it is certain that plasma aldosteron levels are easily affected by a small amount of changes in angiotensin, ACTH, potassium and sodium. However, responses of aldosterone to these changes seem to be decreased in old subjects.
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PMID:[Effects of low salt plus upright posture, angiotensin II, ACTH, and potassium upon plasma renin activity, aldosterone, and cortisol (author's transl)]. 18 65

Angiotensin II, ACTH and potassium chloride were administered to rats for 6 days and the effects on adrenal renin-like activity and adrenal angiotensin II/III immunoreactivity were investigated. Rats infused with angiotensin II (140 pmol/min) either ip or sc showed increases in adrenal angiotensin II/III immunoreactivity (p less than 0.05) and plasma aldosterone concentration (p less than 0.05), but no change in adrenal renin-like activity. Captopril treatment of angiotensin II-infused rats caused a slight decrease in angiotensin II/III immunoreactivity which did not reach statistical significance. In contrast, rats treated with ACTH (Cortrosyn-Z, 3 IU/day, sc) showed an increase in adrenal renin-like activity (p less than 0.01), but no significant change in adrenal angiotensin II/III immunoreactivity. Rats treated with KCl in drinking water showed increases (p less than 0.05) in adrenal renin-like activity, adrenal angiotensin II/III immunoreactivity, and plasma aldosterone. These results suggest that angiotensin II, ACTH and potassium, three major regulators of aldosterone secretion by the adrenal gland, have different effects on the adrenal renin-angiotensin system when administered in vivo.
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PMID:Effects of angiotensin II, ACTH, and KCl on the adrenal renin-angiotensin system in the rat. 215 96

Changes in adrenal renin, which have been regarded as mediator of aldosterone secretion in the adrenal gland, following prolonged ACTH treatment were investigated in male Wistar rats. After 2 days of daily sc injection of ACTH (Cortrosyn-Zinc, 50 micrograms/day), parallel increases in adrenal renin and aldosterone, and plasma aldosterone (PA) were induced. The plasma renin activity (PRA) was slightly but not significantly decreased. Prolonged treatment with ACTH for 8 days increased the adrenal renin, causing a marked reduction in the adrenal aldosterone concentration. The degree of decrease in the PRA was again not significant and similar to that after 2 days of ACTH treatment. Contrary to previout reports which have indicated participation of adrenal renin in the regulation of aldosterone secretion in the adrenal gland, the present results showed reciprocal changes in adrenal renin and aldosterone after prolonged treatment with ACTH. The present findings suggest a complicated relation between adrenal renin and aldosterone secretion in the adrenal gland.
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PMID:Effect of prolonged ACTH stimulation on adrenal renin and aldosterone. 285 39

Spironolactone, a mineralocorticoid antagonist, may also inhibit aldosterone biosynthesis. In vitro studies suggest that spironolactone and its major metabolites inhibit adrenal 18- and 11 beta-hydroxylase activity. We examined various adrenal corticosteroids and their precursors, plasma renin activity, aldosterone excretion rate, and serum and urine electrolytes in normal subjects before and on days 5 and 10 of spironolactone administration (400 mg/day). Plasma corticosteroids were also examined 60 min after ACTH (Cortrosyn) 0.25-mg iv bolus. RIAs were performed after extensive chromatography; there was no interference of spironolactone and its metabolites in the assays. All studies were performed in supine subjects in metabolic balance on a constant 120-meq sodium intake. Plasma renin activity was increased (P less than 0.001) on both days 5 and 10 of spironolactone. Plasma aldosterone (PA) and the aldosterone excretion rate increased (P less than 0.01) on day 5 of spironolactone but decreased (P less than 0.01) from day 5 to 10. Both 11-deoxycorticosterone and 18-hydroxycorticosterone were increased from day 5 to 10. Corticosterone, progesterone, and dehydroepiandrosterone did not increase significantly during spironolactone administration. Incremental PA response to ACTH was less than control on day 10 of spironolactone, but other corticosteroid responses to ACTH were not different during control and days 5 or 10 of treatment. Reduction in PA and further elevation in its precursors during the second 5-day period of spironolactone therapy suggests inhibition of aldosterone biosynthesis during this phase of treatment in normal man. The disproportionate increments in 18-hydroxycorticosterone and 11-deoxycorticosterone suggest biosynthetic inhibition at the 18-dehydrogenase and 11 beta-hydroxylase sites.
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PMID:Plasma corticosteroid concentrations during spironolactone administration: evidence for adrenal biosynthetic blockade in man. 626 60

A 73-year-old man with history of longstanding primary hyperaldosteronism developed adrenal insufficiency after he ruptured an abdominal aortic aneurysm and had a prolonged hypotensive episode. The patient presented as a diagnostic dilemma with recurrent hypotensive episodes and hypokalemia. A cosyntropin (Cortrosyn) stimulation test demonstrated a blunted cortisol response while at the same time having a suppressed plasma renin activity level and an elevated plasma aldosterone value. Diagnosis of Addison disease and concurrent primary hyperaldosteronism resulted in the patient's being treated with an unusual combination of prednisone and spironolactone followed by marked improvement in his symptoms.
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PMID:A patient with concurrent primary hyperaldosteronism and adrenal insufficiency. 1559 30