Concerning the role of arterial baroreceptors in the control of aldosterone secretion.

Since the suggestion by Epstein, Post and McDowell (1) that renal conservation of Na is conditioned by the degree of filling of some portion of the arterial tree, various investigators (2, 4-6) have presented conflicting data concerning the role of arterial baroreceptors in the control of aldosterone secretion. Barger, Muldowney and Liebowitz (3, 5) have suggested that the moderator reflex, of which baroreceptors in the carotid sinus and the aortic arch constitute the afferent limb, may lead to both increased sympathoadrenal tone and hypersecretion of aldosterone in experimental congestive heart failure. Bartter, Gann and Mills (2, 6) have reported that baroreceptors located in the thyrocarotid arterial junction provide the afferent limb of the nervous mechanism that leads to hypersecretion of aldosterone after thoracic inferior vena caval constriction in the dog. Davis, Yankopoulos and Holman (4) have found that neither carotid sinus denervation nor subsequent bilateral vagotomy prevented the increased urinary aldosterone excretion and the virtually complete Na retention observed in dogs with ascites secondary to thoracic inferior vena caval constriction. The present study was designed to examine the hypothesis that arterial baroreceptors play an essential role in the regulation of aldosterone secretion.