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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The in vitro effects of theophylline and aminogluthetimide upon basal and ACTH stimulated cAMP, cortisol and aldosterone responses of normal human adrenocortical tissue were evaluated. Theophylline increased basal cAMP levels and cortisol output, however, basal aldosterone output was depressed. Theophylline in concert with ACTH depressed cortisol and aldosterone output. Aminogluthetimide alone did not affect basal cAMP levels, however, the normal cAMP response to ACTH was delayed in aminogluthetimide pre-treated adrenals. Aminogluthetimide also depressed basal and ACTH stimulated cortisol and aldosterone output with the latter being more sensitive. The findings indicate that both theophylline and aminogluthetimide produce effects upon the adrenal in addition to inhibition of phosphodiesterase and cholesterol side-chain cleavage, respectively. Further, theophylline depression of ACTH stimulated steroid output may be helpful in understanding the interplay between a number of factors in the control of adrenal steroid biosynthesis and release.
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PMID:In vitro effects of theophylline and aminogluthetimide upon basal and ACTH induced cAMP levels and steroid output by the normal human adrenal gland. 20 41

A method of preparing a suspension of cells of the zona glomerulosa from rat adrenal capsules treated with crude collagenase is described. The cells responded to ACTH, angiotensin II and serotonin by increased production of aldosterone. Pooled human sera or individual human sera (from healthy normal or non-psychiatric in-patients) to a final concentration of 30% had no effect on ACTH-stimulated production of aldosterone. Many serum samples from five patients with manic-depressive psychosis, however, caused a reduction in aldosterone production; 65% of those samples taken during depression, 44% of the samples taken during manic episodes and 23% of the samples taken when the mood was normal. Sera from manic-depressive patients also reduced the production of aldosterone caused by angiotensin II or serotonin. This effect of serum from manic-depressives in vitro may be related to the abnormalities of aldosterone control in such patients.
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PMID:Inhibition of aldosterone production in adrenal cell suspensions by serum from patients with manic-depressive psychosis. 21 27

Numerous community drinking water sources have elevated levels of both sodium and lead. Recently reported studies have indicated that elevated levels of sodium in drinking water may be a facter in the development of elevated blood pressure. The question of how elevated levels of lead may affect sodium induced elevated blood pressure is addressed. The hypothesis is developed which states that elevated levels of lead exposure will not interact with sodium to enhance the development of renin angiotensin aldosterone related hypertension but in fact may even diminish the effects of exposure to elevated amounts of sodium on blood pressure through a depression of plasma renin activity.
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PMID:Does exposure to elevated levels of lead enhance sodium induced hypertension? 51 19

The paper describes a two-month period of study in four bipolar manic-depressive patients in a metabolic ward. Plasma renin activity, packed cell volume, plasma sodium and potassium were determined at intervals. Twenty-four-hour urinary sodium, potassium and creatinine were also estimated daily. Aldosterone production rate was measured on two occasions for each patient. Three of the patients showed at least one episode each of mania and depression during the study, while the fourth patient, who was receiving prophylactic lithium throughout, had one ten-day depressive episode but was otherwise normal. No obvious relationship between mood and plasma renin activity was observed, but the group showed a high resting renin activity, a blunted renin response to posture, and inappropriate aldosterone production rates for the renin activity found. It is postulated that a primary defect in the aldosterone-renin system may be present in bipolar manic-depressive psychosis.
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PMID:Renin and aldosterone relationships in manic depressive psychosis. 59 84

In rats, a diet depleted of potassium caused a significant hypokalemia and hypermagnesemia, a diuresis and natriuresis, a decrease in urinary and fecal excretion of potassium, a magnesiuria, and a decrease in fecal excretion of magnesium. Balance studies revealed that potassium metabolism was negative in potassium-depleted rats and that magnesium metabolism was positive and higher than in control rats. In potassium-depleted rats, potassium and magnesium contents in muscle were reduced, whereas the sodium level was increased and plasma aldosterone was significantly lower. Therefore, the elevation in plasma concentration of magnesium induced by a diet poor in potassium is the result of a more positive metabolic balance of magnesium and of shifting of magnesium from the tissue into the plasma compartment. Results of additional preliminary studies support the possibility that the hypermagnesemia may be mediated through the depression in mineralocorticoid activity induced by the depletion of potassium.
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PMID:Magnesium metabolism in potassium-depleted rats. 66 73

Mature and young adult rats were treated with a single dose of 115 mg and 50 mg of pipecolinomethylhydroxyindane (PMHI) maleate per kg of body weight. Large intraperitoneal doses were toxic in mature rats and the growth of younger animals were retarded by the lower subcutaneous dose. In both instances, PMHI caused a rapid reduction in testis weight with arrested spermatogenesis. Atrophic changes to the ventral prostrate and the lowering of blood testosterone levels suggests that the actions of PMHI are not strictly confined to the seminiferous tubules. This was further substantiated by the demonstration of direct inhibition by PMHI of testicular androgenesis in vitro. The actions of PMHI on steroidogenesis may be readily reversible and, compared to tubular actions, are of a minor nature. There were no clear-cut adrenocortical responses to PMHI administration but there was some depression of adrenal gland weight, plasma corticosterone, and aldosterone.
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PMID:Effects of pipecolinomethylhydroxyindane on testicular and adrenocortical function in rats. 73 71

Defective potassium excretion with clinical acidosis, associated with fixed moderate sodium wasting, has been found to be a common abnormality in lead nephropathy. Lead poisoning has been shown by others to be associated with depression of the renin-aldosterone system and of sodium and potassium activated adenosinetriphosphatase (ATPase). Since these hormonal defects may contribute to the hyperkalemia and are reversible, lead poisoning should be treated aggressively. Management also requires proper regulation of dietary sodium, correction of acidosis, limitation of dietary potassium, and minimal use of antihypertensive agents, as well as the administration of allopurinal for urate control.
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PMID:Hyperkalemia and acidosis in lead nephropathy. 94 Oct 56

The effect of prostaglandin E2 on the biosynthesis of corticosteroids was studied in intact rabbits and in the ones with vasorenal hypertension in different periods of its development (1st group) and in the animals subjected to a spurious operation (2nd group). Prostaglandin added to an incubation medium was found to produce in intact rabbits a significant depression of the 11-dehydrocorticosterone and cortisone biosynthesis from progesterone-C14. In rabbits operated upon (1st and 2nd groups) prostaglandin E2 brought changes in the production of corticosteroids no sooner than in 1 month after surgery. In rabbits with vasorenal hypertension brought about through unilateral constriction of the renal artery with an intact second kidney the content of the labeled 11-desoxycorticosterone and 11-desoxycorticosol materially decreased under the effect of prostaglandin E2, while the biosynthesis of the end fractions--11-desoxycorticosterone, aldosterone and cortisone, would gain in intensity. These changes preceded somewhat the most significant rise of the arterial pressure. In the rabbits spuriously operated upon prostaglandin E2 increased the production of corticosteroids and 11-dehydrocorticosterone, low at that time. It is presumed that prostaglandin E2 produces a regulating influence on the processes of the corticosteroids biosynthesis both in normalcy and in vasorenal hypertension.
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PMID:[Changes in the biosynthesis of corticosteroids from progesterone-C14 under the effect of prostaglandin E2 in rabbits with vasorenal hypertension]. 111 13

Experiments were conducted on 30 rats; a study was made of the morphometric and quantitative enzymatico-chemical changes in the glomerular zone of the adrenal cortex in stereotaxic disturbance of the subcomissural organ; there was established a marked atrophy of the glomerular zone, a significant reduction of the diameter of the nuclei of the adrenocorticocytes and depression in these structures of the enzymatic activity of the energy metabolism. Histophysiological characteristics of the glomerular zone can be assessed as its hypofunctional condition and indicates an association between the functional activity of the subcommissural organ and the production of aldosterone.
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PMID:[Influence of destruction of the subcommissural organ on the glomerular zone of the adrenal cortex]. 122 66


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