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)

The administration of the long-acting dopaminergic agonist bromocriptine to five healthy volunteers inhibited the rise in plasma-aldosterone that normally follows the administration of frusemide. This inhibition was not due to a lowering of plasma-renin activity. It is suggested that dopamine may modulate the normal secretion of aldosterone either directly, or indirectly, possible by inhibition of prolactin secretion.
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PMID:Inhibition of the plasma-aldosterone response to frusemide by bromocriptine. 5 77

It has been suggested that prolactin is a regulator of aldosterone secretion. In order to test this hypothesis, we measured prolactin, thyrotrophin and aldosterone by radioimmunoassay and plasma renin activity by the radioimmunoassay of angiotensin I in eight normal women before and after the intravenous injection of 200 microgram of thyrotrophin releasing hormone (TRH). Prolactin increased from 4.1 +/- 1.1 ng/ml (mean +/- SE) to a peak of 27.4 +/- 3.8 (P less than 0.005) at 15 min following TRH. Plasma renin activity was not different from control levels (1.0 +/- 0.2 ng/ml/h) during the first hour following the administration of TRH, nor did the plasma aldosterone concentration differ significantly from the control levels (39 +/- 7 pg/ml) during this period. However, with upright posture, an increase in aldosterone (from 31 +/- 3 pg/ml at 1 h to 68 +/- 9 at 2 h, P less than 0.005) and in plasma renin activity (from 0.9 +/- 0.2 ng/ml/h at 1 h to 2.0 +/- 0.5 at 2 h, P less than 0.05) was noted, demonstrating a normal capacity to secrete aldosterone in these subjects. Similarly, no change in aldosterone was seen in nine patients with primary hypothyroidism given TRH, despite the fact that the increase in prolactin was greater than normal. Chronic hyperprolactinaemia was not associated with hyperaldosteronism in six patients with pituitary tumour. These data demonstrate that acutely or chronically elevated serum prolactin levels do not result in increased plasma aldosterone levels in humans.
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PMID:The relationship between endogenous hyperprolactinaemia and plasma aldosterone. 10 89

Literature on the biochemical effects of oral contraceptives (OCs) is reviewed. The effects of OCs on concentrations of mineral elements ( calcium, phosphorus, magnesium, iron, copper, and zinc), vitamins (ascor bic acid, folic acid, and Vitamins-B6, B12, and E), hormones, (gonadotro pins, progesterone, estrogens, androgens, corticosteroids, aldosterone, renin-angiotensin, insulin, growth hormone, thyroid hormones, catecholamines, and prolactin), amino acids and proteins (free amino acids, tryptophan, metalloproteins, hormone-binding proteins, miscellaneous serum proteins, and blood coagulation factors), carbohydra tes (glucose tolerance tests, glucose metablism and other carbohydrates) , lipids (total serum lipids, triglycerides, phospholipids, fatty acids, and cholesterol), and enzymes (aminotransfereases, alkaline phosphatase, and glutamyltransferase) are reviewed. Changes induced by combined, sequential, and low-dose OCs in 116 biochemical parameters are summarized in a table.
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PMID:Biochemical effects of oral contraceptives. 18 Jul 84

Tonin, an enzyme present in rat submaxillary gland, converts angiotensin I to angiotensin II and is able to form angiotensin II directly from renin substrates. This enzyme was previously shown to be different from renin, tissue isorenins, and angiotensin I converting enzyme. The specific activity of tonin in rat submaxillary gland increases with the age of the animal and is much higher in male than in female rats; this sex difference is apparent from 60 to 70 days of age. There is a sharp drop of tonin activity in hypophysectomized animals, whereas adrenalectomy, thyroidectomy, and gonadectomy have have little effect. The marked increase in tonin activity was observed in animals bearing MtT-F4 transplantable tumors known to produce ACTH, prolactin, and growth hormone. Tonin specific activity in hypophysectomized male rats is restored to control levels by combined treatment with growth hormone and testosterone. Prolactin alone or in combination with testosterone, as well as transplanted pituitaries, has no effect in hypophysectomized animals. There is a significant specific binding of 125I-labeled growth hormone to isolated membranes of rat submaxillary gland.
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PMID:Dependence of tonin activity in rat submaxillary gland on growth hormone and testosterone. 19 8

To investigate whether a direct influence exists between the prolactin suppressive effect of alpha-bromoergocriptine (CB 154) and the aldosterone response to a potassium stimulation, the present study was performed in 7 anephric patients and in 7 non-nephrectomized patients, all on regular haemodialysis. The increase in the plasma potassium concentration between dialysis was used as a stimulus to the adrenals, and was correlated to the increase in the plasma aldosterone concentration (PAC). Plasma samples were obtained during a control period and during a corresponding period of treatment with bromocriptine. Despite a significant fall in the prolactin levels during the bromocriptine treatment, no differences in the aldosterone response to the increasing potassium concentration in the two periods were found neither in the anephric nor in the non-nephrectomized patients. It is concluded that depression of prolactin levels by the dopamine agonist (bromocriptine) has no influence on the ability of the adrenals to react with an increase in aldosterone secretion following potassium stimulation in dialysis patients with and without preserved renin-angiotensin system.
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PMID:Lack of effect of prolactin inhibition by alpha-bromoergocriptine (CB 154) on plasma aldosterone in anephric and non-nephrectomized patients on regular haemodialysis. 19 47

In order to investigate the role of prolactin in the control of the circadian rhythm of plasma aldosterone (PA), plasma renin activity (PRA), cortisol (PC), aldosterone and prolactin (PRL) levels were determined in samples at 4-hour intervals from 5 normal supine men over a period of 24 h under basal conditions and subsequently over a period of 24 h during suppression of prolactin release by bromocriptine (CB-154). After suppression of prolactin, statistically signific1nt circadian rhythms in PC and PA have been detected with a moderate decrease of PA concentration, while the PC level remained unalterated. PRA rhythmicity persisted with a significant shift of acrophase and remarkable reduction of plasma levels. Moreover, during CB administration a significant correlation was obtained between PA and PC, while no correlation was detected between PA and PRA. These data are consistent with the following concepts: (a) the prolactin does not play a significant role in the regulation of circadian rhythm and concentration of plasma aldosterone in normal supine men, and (b) bromocriptine induces a remarkable reduction of PRA and a variable decrease in plasma aldosterone, but it does not influence the secretion of cortisol in normal subjects.
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PMID:Effect of bromocriptine on the control of plasma aldosterone diurnal variation in normal supine man. 22 Jan 71

In pentobarbital-anesthetized dogs, infusion of a low dose of histamine directly into the third ventricle increased plasma ACTH concentration. The increase was unaffected by metiamide, a drug which blocks H2 receptors, but was abolished by mepyramine, a drug which blocks H1 receptors. Mepyramine alone did not produce a decrease in plasma ACTH concentration in stressed dogs. Infusion of the H1 agonist 2-methylhistamine increased plasma ACTH concentration, whereas infusion of the H2 agonist 4-methylhistamine decreased plasma ACTH concentration and blocked the response to surgical stress. Histamine, 2-methylhistamine and 4-methylhistamine had no statistically significant effect on plasma renin activity, blood pressure, or heart rate, and histamine had no effect on plasma prolactin concentration. There were no consistent, specific effects on growth hormone secretion. We conclude that activation of central H1 receptors increases ACTH secretion in dogs, and that activation of central H2 receptors decreases ACTH secretion. Some of the reported effects of cyproheptadine and other drugs on ACTH secretion may be due to their antihistamine activity.
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PMID:Effect of intraventricular histamine on hormone secretion in dogs. 22 2

An increased pressor responsiveness is consistently found in nulliparous patients with gestosis. The following mechanisms may be able to influence arterial reactivity: sodium balance, factors of the kallikrein-bradykinin and the renin-angiotensin systems, an imbalance between vasoconstrictive and vasodilatatory prostaglandins, the sympathetic nervous system, and possibly prolactin, too. A mechanism which is involved in the regulation of uteroplacental blood flow seems to be important in the etiology of gestosis. The immunological changes found in patients with gestosis are insufficient to support the concept of a primary immunopathogenesis. The usefulness of the supine pressor ("roll-over") test, of the angiotensin sensitivity test and serum uric acid determination in predicting hypertensive disorders of pregnancy is evaluated. The supine pressor test is recommended as an appropriate and practical method for routine screening in nulliparous pregnant women.
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PMID:[New aspects of the pathophysiology of gestosis/pre-eclampsia (author's transl)]. 39 81

The effect of TRH induced secretion of TSH and prolactin (hPrl) on plasma renin activity (PRA), water and electrolyte excretion, was studied in 7 normal males before and after an intravenous injection of 2 ml normal saline or 200 microgram TRH. Plasma hPrl and TSH rose significantly (p less than 0.01) in all 7 subjects after TRH but not after saline injection. No significant differences in the hourly excretion of sodium, potassium and free water clearance were noted before and after either saline or TRH injection. Mean PRA values of the 7 subjects were similar after either the 2 ml saline of TRH injection. Our results indicate that despite a correlation between basal hPrl and sodium excretion as well as free water clearance, acute TRH induced elevation of hPrl is not associated with changes of urinary sodium and potassium excretion, free water clearance and PRA in normal males. These findings provide some evidence against a direct osmoregulatory role of hPrl in man.
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PMID:The effects of TRH on prolactin, plasma renin activity, water and electrolyte excretion in normal males. 41 66

This study was designed to investigate the possible role of dopaminergic mechanisms in the control of the renin-angiotensin-aldosterone system in normal man. Six normal male subjects in metabolic balance at 150 meq sodium, 60 meq potassium constant intake received the specific dopamine antagonist, metoclopramide, 10 mg i.v. or placebo followed by angiotensin II infusion 1 h later on 2 consecutive days. Metoclopramide increased plasma aldosterone concentration from 8.2+/-2.2 to 21.0+/-3.3 ng/100 ml (P < 0.005) and plasma prolactin concentration from 18.0+/-4.0 to 91.7+/-4.0 ng/ml (P < 0.001) within 15 min of its administration. At 1 h, plasma aldosterone and prolactin concentrations remained elevated at 16.8+/-2.1 ng/100 ml (P < 0.01) and 86.8+/-15.9 ng/ml (P < 0.005), respectively. Angiotensin II at 2, 4, and 6 pmol/kg per min further increased plasma aldosterone concentration to 27.2+/-3.4, 31.9+/-5.7, and 36.0+/-6.7 ng/100 ml (P < 0.02), respectively. Placebo did not alter plasma aldosterone or prolactin concentrations, but angiotensin II increased plasma aldosterone concentration to 13.7+/-2.4, 19.0+/-1.9, and 23.3+/-3.2 ng/100 ml (P < 0.005). The increment of plasma aldosterone concentration in response to angiotensin II was similar after metoclopramide or placebo. The six subjects also received the dopamine agonist, bromocriptine, 2.5 mg or placebo at 6 p.m., midnight, and 6 a.m. followed by angiotensin II infusion on 2 consecutive d. Bromocriptine suppressed prolactin to <3 ng/ml. After placebo, plasma aldosterone concentration increased from 5.2+/-1.4 to 12.3+/-1.7, 17.2+/-2.2, and 21.8+/-3.5 ng/100 ml (P < 0.01) and after bromocriptine from 7.2+/-1.0 to 14.7+/-3.0, 19.8+/-3.2, and 23.4+/-1.6 ng/100 ml (P < 0.001) with each respective angiotensin II dose. No difference in the response to angiotensin II after bromocriptine or placebo was observed. Plasma renin activity, free 11-hydroxycorticoid concentration, and serum potassium concentration were unchanged by metoclopramide or bromocriptine. The results suggest that aldosterone production is under maximum tonic dopaminergic inhibition which can be overridden with stimulation by angiotensin II in normal man.
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PMID:Effects of metoclopramide and bromocriptine on the renin-angiotensin-aldosterone system in man. Dopaminergic control of aldosterone. 43 33


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