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)

1. The plasma aldosterone responses to exogenous angiotensin II and adrenocorticotropic hormone (ACTH) were studied before and after 1 month of propranolol therapy (120-240 mg/day) in eight patients with essential hypertension. 2. Basal supine plasma renin activity was decreased (P less than 0.001) after propranolol, whereas plasma aldosterone was unchanged. After 3 h of upright posture the increases in both plasma renin activity and aldosterone were decreased (P less than 0.05) after propranolol. 3. Plasma aldosterone responses to exogenous angiotensin II and ACTH were not significantly different after propranolol. Serum and urinary electrolytes and plasma cortisol were also unaffected by propranolol therapy. 4. It is concluded that changes in adrenal sensitivity are not responsible for maintaining unchanged supine plasma aldosterone concentrations after beta-adrenoceptor antagonism in essential hypertension.
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PMID:Effect of propranolol therapy on aldosterone responses to angiotensin II and adrenocorticotropic hormone in essential hypertension. 626 41

The aldosterone response to adrenocorticotropic hormone (ACTH) and angiotensin II (AII) was evaluated in patients with pituitary insufficiency before and after dietary sodium restriction (10 mEq Na+/day for 12 days). On normal sodium intake, plasma aldosterone concentration and plasma cortisol concentration failed to change from control levels in response to a single injection of ACTH or to a continuous 1-hour infusion of AII in patients with pituitary insufficiency. In response to dietary sodium restriction for 12 days, plasma renin activity (PRA) increased fivefold in patients with pituitary insufficiency, while plasma aldosterone concentration failed to increase significantly, averaging 11.0 +/- 3.1 before and 12.3 +/- 3.7 ng/dl (ns, p greater than 0.05) after sodium deficiency. Although aldosterone secretion failed to increase during sodium deficiency, the patients came into balance at 10 mEq without a significant change in arterial blood pressure (BP). In sharp contrast to the lack of aldosterone response to ACTH before sodium deficiency, plasma aldosterone concentration increased markedly from 12.9 +/- 3.3 to 156 +/- 17.3 ng/dl (p less than 0.001) in response to ACTH after sodium deficiency. Although the adrenal glomerulosa cells were markedly sensitive to ACTH during sodium deficiency, they remained almost totally refractory to AII since aldosterone secretion failed to increase significantly in response to continuous infusion of a pressor dose of AII for 1 hour. Replacement therapy with ACTH gel for 3 months in patients with pituitary insufficiency failed to restore a normal aldosterone response to either ACTH or AII. These data demonstrate that some non-ACTH pituitary factor(s) is essential for a normal aldosterone response to ACTH, AII, and sodium deficiency.
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PMID:Regulation of aldosterone biosynthesis during sodium deficiency. Evidence for an essential role of the pituitary gland. 626 60

We describe a premature female infant exposed in utero to danazol during the first trimester of pregnancy. She was first observed in the newborn period with marked degree virilization and clinical findings suggestive of salt-losing congenital adrenal hyperplasia. This was supported by the high plasma levels of 17 alpha-hydroxyprogesterone and adrenocorticotropic hormone and low plasma cortisol level. Levels of testosterone, androstenedione, 11-deoxycortisol, and renin were also elevated. An excessive increase in the levels of 17 alpha-hydroxyprogesterone and 11-deoxycortisol to corticotropin administration associated with impaired increase in plasma cortisol level strongly suggests a partial block in the 21-hydroxylation of 17 alpha-hydroxyprogesterone. However, the high levels of 11-deoxycortisol also suggest a block of the steroid 11 beta-monooxygenase. A year later she was found to have normal basal levels of the adrenal steroids and normal response to corticotropin administration, pointing out the transitory nature of these abnormalities. It may be hypothesized that danazol produced a transitory block of the steroid 21- and 11 beta-monooxygenases in this child.
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PMID:Transient adrenogenital syndrome due to exposure to danazol in utero. 627 Oct 10

1. The blood pressure, renal and metabolic effects of adrenocorticotropic hormone (ACTH) have been studied in six normotensive subjects and two patients with Addison's disease on maintenance steroid therapy. 2. In normotensive subjects, 5 days ACTH treatment (0.5 mg 12 hourly) was associated with a rise in systolic blood pressure and mean arterial pressure. There was a small rise in diastolic pressure but no consistent change in heart rate. Plasma sodium increased and plasma potassium fell. Serum creatinine and urea concentrations were unchanged. Fluid intake increased and urine output was unchanged but ACTH withdrawal was associated with a diuresis. There was an initial reduction in urinary sodium excretion and a natriuresis after ACTH withdrawal. Plasma volume and body weight rose. 3. ACTH produced increases in plasma cortisol, 11-deoxycortisol, corticosterone, deoxycorticosterone, aldosterone, 17 alpha-hydroxyprogesterone and 17 alpha,20 alpha-dihydroxyprogesterone. Plasma renin concentration fell. 4. Patients with Addison's disease showed no change in blood pressure or in any other metabolic variable studied. 5. The effects of ACTH in man resembled those found in sheep.
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PMID:Blood pressure, renal and metabolic effects of ACTH in normotensive man. 627 70

The emotional stress simulated by examinations taken by medical students led to a decrease of sodium concentration in blood. This was a result of a simultaneous increase of mineralocorticoids and a decrease of glucocorticoids responsible for sodium concentration in blood. Both inhibition of glucocorticoids and stimulation of mineralocorticoids were associated with a high activity of plasma renin and a low concentration of adrenocorticotropic hormone.
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PMID:[Role of hormonal compounds in regulating electrolyte metabolism in emotional stress]. 628 76

To determine the effect of hypothermic pulsatile and nonpulsatile cardiopulmonary bypass (CPB) with hemodilution on adrenocortical function we measured plasma levels of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin in two groups of patients. Group I, comprising 11 patients had routine CPB (nonpulsatile), and Group II, comprising 12 patients, had pulsatile flow during CPB (pulsatile). Both groups demonstrated comparable increases in cortisol, ACTH, and aldosterone with operation. Levels for all three hormones appeared to decline during CPB and then rose again in the post-CPB period. There were no significant differences between groups. Plasma renin activity gradually declined in a comparable manner in both groups. In the post-CPB period, renin activity was slightly higher in the nonpulsatile group (1.7 +/- 0.5 versus 0.8 +/- 0.2 ng/ml/hr, p less than 0.05). Correction for the effect of hemodilution demonstrated no decrease in cortisol and a slight increase in ACTH in both groups during CPB. Significant increases occurred in both groups during CPB in urinary Na+ excretion rate and urinary Na+/K+ ratio, more so for the nonpulsatile group. There was no correlation between urinary Na+/K+ ratios and either plasma cortisol or aldosterone levels. Thus routine CPB demonstrates no evidence of adrenocortical hypofunction and the addition of pulsatile flow produces little improvement.
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PMID:Adrenocortical hormone levels during cardiopulmonary bypass with and without pulsatile flow. 629 18

A dopaminergic mechanism has been proposed to suppress aldosterone secretion. To assess the possibility that a defect in the dopaminergic mechanism might enhance aldosterone secretion in hypertensive patients, we determined basal and adrenocorticotropic hormone (ACTH)-stimulated plasma aldosterone (PA), cortisol, renin activity, and potassium concentrations before and during dopamine receptor stimulation with dopamine infusion and bromocriptine administration and dopamine receptor blockade with metoclopramide. The patient study groups included: (a) seven patients with low-renin hypertension and abnormal aldosterone suppression with sodium loading and presumed bilateral zona glomerulosa hyperplasia (ZGHP); (b) two patients with aldosterone-producing adenoma; (c) five patients with low-renin hypertension but normal aldosterone suppression with sodium loading; and (d) six patients with normal-renin hypertension. Dopamine infusion in patients with ZGHP caused PA to fall (P less than 0.01) into the normal range, but did not block the enhanced (P less than 0.05) aldosterone response to ACTH that is characteristic of these patients. Dopamine infusion in patients with low-renin hypertension but normal aldosterone suppression also suppressed PA (P less than 0.01), whereas it had no effect upon PA in patients with normal-renin hypertension or aldosterone-producing adenoma and did not blunt the PA response to ACTH in either group. Bromocriptine administration had no effect upon basal or ACTH-stimulated PA. Dopamine infusion in patients with ZGHP also enhanced (P less than 0.05) diuresis and natriuresis in comparison with normal-renin patients. Metoclopramide administration increased (P less than 0.01) PA in all patients. Thus, a dopaminergic mechanism appears to be important in the regulation of aldosterone secretion in patients with ZGHP and in other low-renin hypertensives with normal aldosterone suppression with sodium loading. In contrast, this latter group does not exhibit an enhanced aldosterone response to ACTH. Both of these groups differ from normal-renin hypertensives, who have no PA suppression with dopamine infusion.
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PMID:Aldosterone suppression with dopamine infusion in low-renin hypertension. 630 9

Studies were performed in anesthetized dogs to investigate the mechanism of the suppression of vasopressin and adrenocorticotropic hormone (ACTH) secretion by clonidine. Injection of clonidine (30 micrograms/kg i.v.) produced an initial increase in arterial pressure followed by hypotension, decreased heart rate, increased right atrial pressure and decreased plasma renin activity. Plasma vasopressin concentration decreased from 14.6 +/- 3.0 to 2.2 +/- 0.4 pg/ml (P less than .01), and this was accompanied by increases in urine volume and free water clearance from 0.15 +/- 0.02 to 1.03 +/- 0.28 and -0.50 +/- 0.05 to 0.30 +/- 0.27 ml/min, respectively (P less than .01), and a decrease in urinary osmolality from 1450 +/- 124 to 372 +/- 97 mOsmol/kg of H2O (P less than .01). Plasma corticosteroid concentration, used an an index of ACTH secretion, decreased from 8.9 +/- 1.6 to 2.2 +/- 0.3 micrograms/dl (P less than .01). Plasma osmolality did not change. Pretreatment of dogs with the alpha adrenoceptor antagonist yohimbine (2 mg/kg i.p.) blocked all cardiovascular, endocrine and renal responses to clonidine. Bilateral cervical vagotomy did not block the suppression of vasopressin or corticosteroid secretion by clonidine. Intraventricular injection of yohimbine blocked the hypotension and suppression of plasma corticosteroid concentration produced by clonidine but did not block the decrease in plasma vasopressin concentration or the associated renal effects of clonidine. Intracarotid infusion of clonidine caused small decreases in plasma vasopressin and corticosteroid concentrations even though blood pressure decreased by 22 mm Hg. Intraventricular and intravertebral clonidine had no significant effect on plasma vasopressin or corticosteroid concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of suppression of vasopressin and adrenocorticotropic hormone secretion by clonidine in anesthetized dogs. 632 82

The stimulatory effect of metoclopramide upon aldosterone secretion is independent of the known aldosterone-regulating mechanisms (renin, potassium, adrenocorticotropic hormone), is unrelated to its effect on prolactin and is absent when metoclopramide is directly added to isolated adrenal zona glomerulosa cells. To examine the possibility of a "humoral" mediation of aldosterone stimulation by metoclopramide, we evaluated the effect of serum of 10 normal subjects injected with metoclopramide (10 mg i.v.) on aldosterone production by collagenase-dispersed calf adrenal zona glomerulosa cells. Whereas no effect was observed with serum collected before the injection, serum collected from 5 to 30 min after the injection stimulated aldosterone production. The effect was seen 2.5 min after the injection, was significant at 5 min (P 0.05), 10, 15, 20 and 30 min (P 0.01). The effect disappeared 40 min after the injection, when plasma aldosterone in subjects was still elevated (P 0.01). The biological half-life of the factor (t1/2) is about 12.5 min. A significant correlation was found between the maximal aldosterone response to metoclopramide in vivo and the maximal effect of serum in vitro (r2=0.69;P 0.01). We suggest that metoclopramide stimulates aldosterone production in vivo by the increase in serum of a factor which, in turn, stimulates aldosterone and whose physiological significance remains to be evaluated.
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PMID:Evidence for a role of a serum factor stimulated by metoclopramide in regulating aldosterone secretion. 670 35

The purpose of this study was to examine the effect of circulating androgens on neuroendocrine, autonomic, and behavioral responses to stress. The effects of conditioned stress were studied in male Sprague-Dawley rats that were intact, gonadectomized, or gonadectomized and treated with dihydrotestosterone (DHT). Intact animals received sham surgeries. Animals were stressed 3 wk after surgery. The adrenocorticotropic hormone (ACTH) response to conditioned stress was significantly potentiated (P < 0.01) in gonadectomized males compared with sham-operated and gonadectomized DHT-treated animals. In stressed rats, plasma corticosterone levels were significantly higher (P < 0.05) in gonadectomized animals compared with DHT-treated castrates. The prolactin response to stress was decreased (P < 0.01) in gonadectomized males compared with sham-operated and gonadectomized DHT-treated rats. The stress-induced increases in plasma renin activity and concentration were not altered in gonadectomized or in gonadectomized DHT-treated animals. Nonstressed DHT-treated castrates exhibited more "fearlike" behavior compared with nonstressed sham-operated and gonadectomized animals. However, conditioned stress produced the same behavioral effects in all treatment groups. The results demonstrate that the ACTH/corticosterone, prolactin, and behavioral responses to a psychological stressor are differentially regulated by circulating androgens.
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PMID:Castration attenuates prolactin response but potentiates ACTH response to conditioned stress in the rat. 748 3


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