Hypertensive effect of 17α, 20α7–dihydroxyprogesterone and 17α-hydroxyprogesterone in the sheep

Abstract

ANIMAL experimental models of high blood pressure as caused, for example, by renal artery constriction or administration of mineralocorticoid hormones and salt, have yielded basic data on physiological processes which have helped in the diagnosis and treatment of human hypertension. The discovery that ACTH administration causes a reproducible hypertension of rapid onset in the sheep provided a new model for analysis^1,2. Certain clinical observations have indicated that there may be as yet unidentified steroids which are causally involved in some hypertensive states: for example, instances of high blood pressure in children and adults which were corrected by dexamethasone treatment^3,4, and reversal of high blood pressure in the low renin group of essential hypertensives by inhibitors of steroidogenesis or by spironolactone have been described^4–6. We report here the hypertensive effect of 17α, 20α-dihydroxyprogesterone (17α, 20α-diOHP; 17α, 20α-dihydroxy-4-pregnene-3-one) and 17α-hydroxyprogesterone(17α-OHP) in sheep made hypertensive with ACTH. These two progesterones were identified in the adrenal venous effluent from ACTH-hypertensive sheep and were shown to be secreted in greatly increased amounts.