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The response of plasma renin activity (PRA) to sodium restriction, furosemide and ACTH administration were studied in six patients with panhypopituitarism of various causes and in a patient with Addison's disease. In all the patients with panhypopituitarism, the basal levels of PRA were within normal limits and the responses of PRA and sodium homoeostasis to sodium restriction and furosemide administration were not significantly different from those of normal subjects. On the other hand, in an Addisonian patient the basal level of PRA was very high and this was further increased with a decrease in the serum level of sodium and an increase in the serum level of potassium after one day of sodium restriction. The administration of 1 mg of synthetic β1–24 ACTH every 12 hours for 2 days caused an increased plasma 11-OHCS and urinary 17-OHCS. with a decrease of sodium and an increase of potassium loss in the urine but failed to change PRA in patients with panhypopituitarism. In the Addisonian patient, ACTH did not influence the levels of plasma 11-OHCS, urinary 17-OHCS, PRA as well as serum and urinary electrolytes. From these results it is suggested that ACTH does not directly act on renin secretion and that PRA can adequately respond to various stimuli such as sodium restriction and furosemide administration in a condition of ACTH deficiency.

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ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.