Pathogenesis of hypertension in Cushing's syndrome

L. Krakoff, G. Nicolis, B. Amsel

Research output: Contribution to journalArticlepeer-review

97 Scopus citations

Abstract

Steroid production, plasma renin activity (PRA) and plasma renin substrate (PRS) were measured in eight patients with hypertension due to Cushing's syndrome of benign origin. Despite elevation of cortisol secretion in all patients, hypokalemia and suppressed PRA was noted in the one subject with a functioning adrenal adenoma. PRA was normal in six patients on an unrestricted sodium intake but was markedly increased in the two patients on low salt diets. PRS was significantly increased during active disease, but decreased substantially with treatment. The absence of uniform hypokalemia and of suppression of renin indicates that mineralocorticold production could not account for the increase in arterial pressure. It is suggested that glucocorticoid-induced hypertension may be initiated by alterations in vascular responsiveness to pressor agents and that elevated PRS levels may contribute to increased angiotensin formation.

Original languageEnglish
Pages (from-to)216-220
Number of pages5
JournalAmerican Journal of Medicine
Volume58
Issue number2
DOIs
StatePublished - Feb 1975

Fingerprint

Dive into the research topics of 'Pathogenesis of hypertension in Cushing's syndrome'. Together they form a unique fingerprint.

Cite this