CONCERNING THE ROLE OF ARTERIAL BARORECEPTORS IN THE CONTROL OF ALDOSTERONE SECRETION

Abstract

Extensive denervation of the central arterial tree, including both the cervical carotid and the aortic arch baroreceptor areas, failed to prevent the hypersecretion of aldosterone and virtually complete Na retention that results from thoracic inferior vena caval constriction in the dog, and superimposed bilateral vagotomy and bilateral splanchnic nerve section did not affect the increased secretion of aldosterone observed in these animals. After the denervation procedures, acute hemorrhage in one dog resulted in an increase in the rate of aldosterone secretion which was similar to that observed following hemorrhage in dogs with intact baroreceptor areas. Bilateral low cervical carotid arterial constriction resulted in a,n increase in aldosterone production in 2 of 7 dogs; in both animals, the change appeared to be mediated via increased ACTH release. Simultaneous constriction of the celiac axis and the superior mesenteric artery had no effect on aldosterone secretion. These data offer no support for the concept that arterial baroreceptors constitute the afferent limb of a reflex arc concerned with the primary regulation of aldosterone secretion.