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In addition to reviewing evidence bearing on the broad relationship of adrenal and electrolyte changes to the pathogenesis of hypertension, this conference considered more specifically the changes in vascular reactivity and electrolyte excretion in hypertension. Supporting the theory of an adrenal mechanism in hypertension was evidence that the development of adrenal-regeneration hypertension in different species may bear a direct relationship to the degree of adrenal regeneration (Dr. Skelton), and that a steroid having electrolyte action opposite to that of desoxycorticosterone is hypotensive in action both in DCA and renal ischemic hypertension, but not in normotensive animals (Dr. Sturtevant). On the other hand, it was observed that adrenalectomy does not alter the development of hypertension produced by kidney encapsulation in the rat (Dr. Fregly). Although it is probable that constrictor agents cause a greater increment in vascular resistance in hypertension than in normotension, the interpretation of this relationship in terms of responsiveness of vascular smooth muscle is fraught with difficulties: 1. The base line of vascular resistance in hypertension is different from that in normotension, and it is possible that the increment in resistance for a given amount of smooth muscle shortening is greater in the constricted than in the normal vessel (Dr. Tobian). 2. It is possible that the increase in resistance in hypertension is due to the encroachment of the edematous blood vessel wall into the lumen without an increase in tone of vascular smooth muscle (Dr. Tobian). 3. The responsiveness to epinephrine of aortic strips from hypertensive animals is less than (Dr. Bohr) or no greater than (Dr. Tobian) that from the nor mal animal. The pertinence of the aortic strip studies was questioned, both because the aorta differs in function (Dr. Sancetta) and responsiveness (Dr. Bohr) from the arteriole and because epinephrine was used in these studies (Dr. Skeggs). The problem of tachyphylaxis of the isolated artery strip in response to angiotonin may not yet be resolved (Drs. Bohr and Helmer). In hypertension there is an increase in sodium excretion by the kidney which is accentuated by the administration of a sodium chloride load. This abnormality reflects an impairment of the tubular reabsorption of sodium which is related to an impaired reabsorption of water (Dr. Sapirstein) and is a direct function of the arterial blood pressure (Drs. Hollander and Weller).

Conference on Electrolyte and Adrenal Factors in Human and Experimental Renal Hypertension