Hypertensive Vascular Disease Induced by Heterologous Renin

Abstract

Chronic treatment with crude hog, or rat, renin administered subcutaneously to uninephrectomized rats elicits hypertension, renal and vascular lesions, hypertrophy of the zona glomerulosa of the adrenals, and renin depletion in the remaining kidney. Semipurified hog renin given in equipressor doses also causes renin depletion and stimulation of the zona glomerulosa, but no hypertension nor vascular disease. However, semipurified hog renin becomes as effective as the crude preparation after addition of retarding substances such as gelatin, oil, or cholesterol. Thus, a prolonged and sustained resorption of renin seems to be a prerequisite for the development of hypertension. Since hypertension takes place only after a latent period during which arterial pressure remains within the normal range, it does not appear that hypertension can be attributed to the acute pressor effect of renin. It is proposed as a working hypothesis that renin, through angiotensin, initiates nervous mechanisms which are responsible for the development of benign hypertension and that the acute pressor effect of angiotensin is more specifically associated with the malignant phase of hypertension.