Chronic effects of carotid sinus denervation, cervical vagotomy and aortic depressor nerve section on aldosterone and sodium excretion.

Abstract

Carotid sinus denervation in dogs and aortic depressor nerve section in rabbits were without effect on urinary aldosterone and sodium (Na) excretion. Also, adrenal vein aldosterone output following both acute and chronic carotid sinus denervation was unaltered. Constriction of the thoracic inferior vena cava in dogs with carotid sinus denervation resulted in hyperaldosteronuria, marked Na retention and ascites, a response in no way different from that occurring in intact dogs. Subsequent unilateral cervical vagotomy had no detectable influence on the hyperaldosteronism and Na retention. Section of the remaining vagus resulted in a slight increase in Na excretion, but Na balance remained positive and ascites continued to accumulate. Since the increase in Na excretion was meager and the continued high rate of aldosterone output occurred in two of three dogs, it seems unlikely that the vagus constitutes an appreciable part of an afferent nervous limb. The data offer no support for the concept that receptors concerned with the control of aldosterone secretion or Na excretion are located in the aortic arch or carotid sinus.