ADRENAL CORTICAL FUNCTION IN HYPERTENSION

Abstract

THERE is an impressive body of suggestive evidence for the importance of the adrenal cortex in various types of hypertension. The subject has been comprehensively reviewed by Sapeika (1) and Perera(2). In the present communication, some of the relevant clinical and experimental observations will be briefly recapitulated in order to place this investigation in its proper perspective. Pressor effects of desoxycorticosterone esters have been demonstrated in various animals (3, 4), and morphologic changes were first described by Selye et al. (5). These included generalized vascular lesions similar to those seen in human nephrosclerosis and in malignant hypertension. Subsequently, studies by Knowlton et al. (6), employing much lower dosages in rats, revealed no significant vascular lesions; but in nephritic rats (the nephritis being induced by cytotoxic serum) striking hypertension was readily induced. The development of these lesions can be inhibited by simultaneous administration of glucocorticoids or ACTH (7, 8). Loeb et al. (9) first reported hypertension in 2 patients suffering from Addison's disease, who were treated with desoxycorticosterone esters. This pressor effect has also been demonstrated in uncomplicated hypertensive vascular disease, but not in normotensive subjects (10). The elevation was masked by salt withdrawal and apparently blocked by simultaneous administration of adrenal cortical extract (11). Cortisone in a dose of 200 mg. per day was found to cause a small but definite depression of the blood pressure in a patient with hypertensive vascular disease, which persisted for several weeks after cortisone had been discontinued (12).