The Soffer test in essential hypertension.

The hypertension occurring in association with adrenal cortical hyperfunction (Cushing's syndrome and congenital adrenal hyperplasia), the difficulty in establishing or maintaining experimental hypertension in the absence of the adrenal gland (1-3), and the amelioration of human "essential" hypertension by adrenalectomy (4) or the development of adrenal insufficiency (5) have led several investigators (6-8) to suggest that adrenal hyperfunction might contribute to the pathogenesis of human "essential" hypertension. Attempts by a number of investigators to demonstrate this hyperfunction have been unsuccessful. Selye (9), Bruger, Rosenkrantz and Lowenstein (10), and Daughaday, Jaffe and Williams (11) have found the analysis of metabolic excretory products of the adrenal cortex (17-ketosteroids and 11-oxysteroids) in the urine of patients with hypertension to yield normal or low values. Careful study of carbohydrate metabolism in patients with hypertension (12) by means of the insulin tolerance test has revealed no abnormalities. Nitrogen balance is easily maintained in hypertensive subjects with a small protein intake (13). We and others (14) have found the blood eosinophil count normal in hypertension. Schroeder, Davies and Clark (15) have shown that the excretion of sodium in the sweat is normal in ordinary essential hypertension. The renaissance of interest in the therapeutic efficacy of a low sodium regime in the treatment of hypertension has focused attention particularly on the electrolyte controlling properties of the adrenal cortex as a possible mechanism for adrenal contribution to the pathogenesis of hypertension. The plasma electrolyte abnormality (hypochloremic alkalosis) frequently seen in Cushing's syndrome is not seen in hypertension. Most observers have found no plasma electrolyte abnormality in hypertension although Selye (9) believes the ratio of sodium to chloride is high. Soffer and his associates (16, 17) have pointed out that patients with Cushing's syndrome have an abnormal response to salt loading and the administration of desoxycorticosterone. His normal individuals, after a given salt load, retained more of the salt after the administration of desoxycorticosterone than they did without this drug. On the other hand, the patients with Cushing's syndrome showed an increased "diuresis" of the salt load after desoxycorticosterone. This observation has been confirmed by others (18, 19). It is conceivable, then, that should patients with essential hypertension have adrenal cortical hyperfunction with respect to electrolyte metabolism they would exhibit this same abnormal response.