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 peripheral blood concentrations of aldosterone, corticosterone and cortisol were measured during pregnancy in conscious, undisturbed sheep. 2. Aldosterone levels did not change during pregnancy and the mean pregnant value, 1-2 s.d. 1-4 ng/100 ml(n = 12) was not significantly different from the non-pregnant value, 2-1 s.d. 1-7 (n = 16). 3. Cortisol levels likewise were unchanged by pregnancy-non-pregnant values were 0-56 s.d. 0-50 mug/100 ml (n = 12) compared with 0-46 s.d. 0-40 mug/100 ml (n = 16) in pregnant sheep. 4. Sheep of 110-140 days gestation had a 400 mmol greater total exchangeable sodium than non-pregnant sheep. Plasma volume and plasma renin concentration tended to be elevated near to term. 5. Very high aldosterone secretion rates and peripheral blood levels could be produced in pregnant sheep by stress, intravenous ACTH or angiotensin II infusions, and by sodium deficiency. It is suggested that the pregnant sheep may show increased sensitivity in contrast to non-pregnant sheep to these stimuli and the enlarged size of their adrenals may be a contributing factor.
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PMID:The effect of pregnancy on mineralo- and gluco-corticoid secretion in the sheep. 18 93

The effects of transcendental meditation (TM) on plasma renin activity (PRA) and plasma concentrations of aldosterone, cortisol, and lactate were studied by measuring these variables before, during, and after 20--30 min of meditation. Subjects, who rested quietly rather than meditating, served as controls. There were no differences in the basal values for these variables between meditators and controls, but controls, in contrast to meditators, showed a significant increase in cortisol between the first (A) and second (B) samples of the control period. PRA increased slightly (14%) but significantly (p less than 0.03) during TM, but not during quiet rest in controls. Cortisol decreased progressively (after sample B) throughout the experiment to the same degree in both groups. Aldosterone and lactate did not change. The data do not support the hypothesis that TM induces a unique state characterized by decreased sympathetic activity or release from stress, but do suggest that meditators may be less responsive to an acute stress.
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PMID:Renin, cortisol, and aldosterone during transcendental meditation. 37 2

Tryptophan administration was used to evaluate the possibility that serotonergic neurons are involved in regulating the release of cortisol, renin, and aldosterone. Eleven studies were undertaken using 2 or 10 g tryptophan administered to fasting patients in continued supine posture. Aldosterone rose significantly to 208% (range, 128-329%) of baseline in all seven studies using 10 g and in one of the four studies using 2 g. Renin rose significantly to 189% (range, 116-340%) of baseline in four of the seven studies using 10 g and in two of the four studies using 2 g. Cortisol rose from 10.1 +/- 3.3 to 20.0 +/- 3.7 micrograms/100 ml (P less than 0.001 by t test) in six of the seven studies using 10 g and three of the four studies using 2 g. In eight studies, there was a significant rise of more than one substance after tryptophan administration. In six of these, peak values of the responding hormones occurred at the same time or within a single 30-min sampling interval despite the absence of a constant relationship between their rises. The results suggest participation of the central serotonergic nervous system in the control of renin and aldosterone in addition to its previously postulated role in cortisol release.
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PMID:Stimulation of aldosterone, renin, and cortisol by tryptophan. 42 5

Biochemical investigations in a boy with a salt losing syndrome revealed a very low secretion of aldosterone which did not rise during salt deprivation, in spite of a normal rise in plasma renin activity. Cortisol secretion was normal - but subsequently decreased, while the corticosterone secretion was high. The patient was studied at the age of 5 weeks, 3 months and also at the age of 8 months. He survived until the age of 18 months on treatment with sodium chloride and DOCA, but did not receive glucocorticoids. At autopsy the adrenal glands were absent, but in fat tissue from the upper renal poles foetal adrenal cortex tissue was found. The histological picture agrees well with other cases which could be designated as "foetal-cortex-only" adrenal hypoplasia. The same histological changes were demonstrated in the boy's brother who died suddenly at the age of 6 weeks. The boy's testes were advanced in maturation to a stage of about ten years: spermatocytes and Leydig cells were present.
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PMID:Familial adrenocortical hypoplasia with early clinical and biochemical signs of mineralocorticoid deficiency (hypoaldosteronism). 57 34

Plasma Aldosterone (PA) response to metoclopramide (10 mg i.v.) was studied in 11 normal, 2 hypophysectomized subjects and in one patient with bilateral adrenal hyperplasia. All the subjects were kept on a normal sodium and potassium intake. Four normal subjects were pretreated with 1 mg of dexamethasone in order to inhibit endogenous ACTH. In all subjects metoclopramide elicited a prompt rise of PA comparable to that obtained with angiotensions or ACTH. No significant change of blood pressure, serum electrolytes, plasma renin activity, Plasma Cortisol (PC) was detected. The lack of PC response to metoclopramide and the PA increase in dexamethasone pretreated subjects rule out an ACTH mediated effect. The increase of PA in hypophysectomized subjects, in whom metoclopramide did not stimulate any prolactin release, rules out a prolactin mediated effect. Metoclopramide increases plasma aldosterone concentration probably via a direct action on the adrenal glomerular zone or throught another unknown mechanism.
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PMID:Metoclopramide increases plasma aldosterone concentration in man. 59 26

The renin-angiotensin system, ACTH and hyperkalaemia are known to induce increased plasma levels of aldosterone. In order to assess the relative significance of these mechanisms during surgical stress, aldosterone, cortisol and electrolytes in plasma were measured in 12 otherwise healthy women during and after cholecystectomy. The patients received either isotonic sodium chloride or 5 per cent glucose in water during the experimental period of 22 h. The results showed that the pronounced increase of aldosterone and the concomitant decrease of sodium in plasma found in patients given glucose in water could almost be inhibited by the administration of saline. Cortisol and potassium concentrations were identical in the two groups of subjects. It is concluded that the aldosterone response to surgery is mainly mediated via the renin-angiotensin system. This response is probably due to a reduced sodium content or volume of extracellular fluid, since it could almost be inhibited by administration of sodium chloride. The rationale of saline restriction during and after surgery is questioned.
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PMID:Inhibition of aldosterone response to surgery by saline administration. 63 42

Hormone, electrolyte, and body fluid compartment changes were studied in subjects who either spent time at 10,000 ft before flying to 17,500 ft or were premedicated with acetazolamide and flown directly to 17,500 ft. In the former group, at 10,000 ft, renin and aldosterone were not different from control. Cortisol increased significantly from 9.8 to 19.5 mug/100 ml on the third day. At 17,500 ft, renin, aldosterone and cortisol were significantly elevated on day 3 but had returned to control levels by day 5. Sodium and potassium excretion was significantly reduced at both altitudes. Total body water, extracellular and plasma volume were reduced (P less than 0.05) at 17,500 ft. Subjects pretreated with acetazolamide and flown directly to 17,500 ft had significant increases (P less than 0.001) in plasma renin, aldosterone, and cortisol levels during the first 4 days at altitude. On day 1 there was a decrease of 45% in sodium and 38% in potassium excretion. On day 4 there was a decrease of 63% and 51%, respectively. These changes are not associated with the premedication. The initial changes may reflect the immediate response to stress and alkalosis followed by a return to control levels as the body adapts to altitude.
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PMID:Hormonal and electrolyte response to exposure to 17,500 ft. 114 Oct 94

Peak exercise capacity (Peak VO2), neurohormonal changes, ventricular enlargement and ejection fraction are among the most important determinants of prognosis in congestive heart failure. However, the inter-relation between these parameters is unknown. We, therefore, correlated these indices in patients with hemodynamically severe congestive heart failure (NYHA class II, pulmonary artery wedge pressure 25 +/- 2 mm Hg, cardiac index 2.5 +/- 0.2 l/min/m2, ejection fraction 43 +/- 2% and fractional shortening 19 +/- 1%). Peak VO2 measured directly during exercise by breath to breath expiratory gas analysis using a metabolic cart was 23 ml/min/kg. Plasma epinephrine (E) and norepinephrine (NE) were measured by high performance liquid chromatography (HPLC) and plasma renin activity (PRA), aldosterone (Aldo), cortisol, prolactin, growth hormone, anti-diuretic hormone (ADH) and antinatriuretic peptide (ANP) by radioimmunoassay. Ejection fraction was measured by echocardiography. There was no relation between peak VO2 and any of the neurohormones E: r = -0.43, NE: r = -0.43, ANP: r = -0.49, Cortisol: r = -0.37, ADH: r = -0.07, Aldo: r = -0.45, 2 tail critical value 0.55. PRA showed a modest correlation (r = -0.61). Similarly, there was no relation between ejection fraction or degree of ventricular enlargement and any of the other indices (r = -0.05). We conclude that although peak VO2, neurohormonal profile and ventricular function are important individual prognostic determinants, there seems to be no direct relation between them.
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PMID:Relation between major indices of prognosis in patients with chronic congestive heart failure: studies of maximal exercise oxygen consumption, neurohormones and ventricular function. 128 16

The lack of a nocturnal decrease in blood pressure in cyclosporine-treated cardiac transplant recipients may indicate abnormalities in the mechanism(s) responsible for circadian variability in other physiologic parameters such as in circulating hormones. This possibility was addressed through repeated determinations of circulating catecholamines, neuropeptide Y, pancreatic polypeptide, calcitonin gene-related peptide, plasma renin activity, aldosterone, atrial natriuretic factor and cortisol. The results from 10 patients with heart transplants were compared with those of 12 age-matched, healthy control subjects. Both groups were studied during 24-hour supine rest. There was no difference between patients and control subjects in mean levels of catecholamines, neuropeptide Y, pancreatic polypeptide and aldosterone. Patients had higher levels (+/- SD) of plasma renin activity (6.4 +/- 1.3 vs 2.6 +/- 0.4 ng/ml/hour, p less than 0.001), calcitonin gene-related peptide (47.7 +/- 9.9 vs 33.3 +/- 5.7 pmol/liter, p less than 0.01) and atrial natriuretic factor (93.0 +/- 56.7 vs 20.7 +/- 8.9 pg/ml, p less than 0.001) than control subjects, respectively. Cortisol was not detected in patients. Abnormal diurnal profiles in patients were found for calcitonin gene-related peptide, aldosterone and atrial natriuretic factor, and for pancreatic polypeptide, together with decreased levels, in patients with greater than 6 months follow-up. Except for hormones reflecting sympathetic nervous activity, all hormonal systems studied showed abnormalities in level or circadian rhythmicity, or both. The pancreatic polypeptide results suggest that parasympathetic neuropathy could develop in cyclosporine-treated heart transplant recipients.
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PMID:Level and diurnal variations of hormones of interest to the cardiovascular system in patients with heart transplants. 153 Nov 62

Sodium nitroprusside was infused intravenously for 10 minutes in normal men, reclining at 45 degrees, in a dose sufficient to decrease the arterial pressure by 10 mmHg. The effect on a variety of plasma hormones was measured during the infusion and for 20 minutes afterwards. The heart rate increased to a maximum of 149%. Norepinephrine rose to a maximum of 196% in 5 minutes. Epinephrine reached a peak of 207% after 10 minutes. Plasma renin activity reached a peak of 449% at 10 minutes. Aldosterone did not change during the infusion, but increased to a maximum of 145% 10 minutes later. Vasopressin increased sharply at the end of the infusion to 893% and then rapidly decreased. Corticotropin, prolactin and growth hormone started to increase toward the end of the infusion, but reached their maxima during recovery. Corticotropin (225%) and prolactin (288%) peaked 10 minutes after the infusion, while growth hormone (414%) appeared still to be rising 20 minutes after the end of the infusion. Cortisol also rose progressively during recovery to a level of 138%. No significant changes were seen in the concentrations of insulin, glucagon, atrial natriuretic peptide, bombesin or neurotensin.
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PMID:Temporal relations of the endocrine response to hypotension with sodium nitroprusside. 155 71


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