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Biomedical subjects

E N Ehrlich

Publications and source records attributed to E N Ehrlich.

At least 37 records · Page 2Linked to original sources
PubMed1975

Effect of progesterone on renal sodium handling in man: relation to aldosterone excretion and plasma renin activity.

1. The effect of progesterone on renal haemodynamics and intrarenal sodium handing was evaluated in thirteen normal men on a constant diet. Clearances were measured during maximal water diuresis and again 4-7 days later, this time 3 h after progesterone was given intramuscularly. Seven additional studies were performed 3 days after progesterone administration. Another four tests were performed on volunteers who had manifested renal 'escape' from the sodium-retaining effect of deoxycorticosterone acetate. 2. In acute progesterone studies glomerular filtration rate was unchanged, whereas effective renal plasma flow increased, so that filtration fraction decreased significantly. A similar in crease in urinary sodium occurred whether subjects received a low or high sodium diet. Indices which related to the distal delivery of filtrate (fractional urine flow and the sum of fractional free water and sodium clearances) increased significantly in both groups. The progesterone-induced increase in sodium excretion was not related to changes in plasma renin activity, renin substrate or urinary aldosterone. After 3 days of progesterone, the increase of sodium excretion was less than in the acute studies and urinary aldosterone increased tow- to four-fold. Progesterone failed to produce an acute increse in urinary sodium in subjects hyperexpanded by administration of exogenous mineralocorticoids. 3. Results suggest that the acute natriuretic action of progesterone is in part independent of aldosterone inhibition and that progesterone may inhibit sodium reabsorption at proximal as well as distal sites in the nephron.

Adult↗
PubMed1972

Effect of administered mineralocorticoids or ACTH in pregnant women. Attenuation of kaliuretic influence of mineralocorticoids during pregnancy.

The role of augmented aldosterone production in pregnancy is poorly understood. Whereas some consider aldosterone secretion in pregnancy excessive, others suggest that this is a compensatory phenomenon. According to yet another view, mechanisms other than the renin-angiotensin-aldosterone system control sodium homeostasis in pregnancy. Metabolic balance studies were performed on 14 3rd trimester women. Mineralocorticoid activity was experimentally increased by administering desoxycorticosterone acetate, 9alpha-fluorocortisol acetate, or ACTH for 4-12 days. Administration of mineralocorticoid or ACTH consistently caused sodium retention. During this mineralocorticoid-induced volume expansion, aldosterone excretion decreased markedly. Natriuresis, which followed discontinuance of the drug, continued while aldosterone excretion, although greatly diminished compared to control values, was greater than that found in normal, nonpregnant individuals. This saline diuresis did not subside until aldosterone excretion returned to its previously high control values. These observations support the concept of the physiological role of increased aldosterone production in pregnancy. Results further revealed a marked dissociation between antinatriuretic and kaliuretic effects of corticoids. Potassium balance was virtually unaltered during continued mineralocorticoid or ACTH administration, despite initially high or abruptly increased sodium intakes. Finally, mineralocorticoid escape was induced by continued desoxycorticosterone acetate therapy in two male volunteers. Kaliuresis occurred which was subsequently abolished when progresterone was administered. Sodium excretion, however, was virtually unaltered. These data, mimicking results observed in gravidas, suggest that progesterone is an important determinant of potassium homeostasis in pregnant women.

Adolescent↗