Role of cardiac output and the autonomic nervous system in the antinatriuretic response to acute constriction of the thoracic superior vena cava.

Abstract

Studies were performed on anesthetized saline-loaded dogs to delineate the afferent and efferent mechanisms involved in the antinatriuretic response to acute constriction of the thoracic vena cava. The kidneys of the animals were denervated prior to study, and renal perfusion pressure was controlled throughout the experiment. To differentiate between the potential afferent stimuli, increased hepatic venous pressure and decreased cardiac output, the thoracic superior vena cava (TSVC) was acutely constricted to lower cardiac output without increasing hepatic venous pressure. Acute TSVC constriction caused a decrease in sodium excretion qualitatively similar to that resulting from an acute constriction of the thoracic inferior vena cava (TIVC) which generated a comparable decrease in cardiac output. This finding suggests that the afferent limb of the antinatriuretic response to acute constriction of the thoracic vena cava, either TSVC or TIVC, involves diminution in cardiac output, or some consequence thereof, rather than increased hepatic venous pressure. Additional experiments were then performed in animals with pharmacologically-induced autonomic blockade. Autonomic blockade with hexamethonium or phenoxybenzamine abolished the antinatriuretic response to constriction of either the TIVC or TSVC. This finding suggests that the efferent limb of the antinatriuretic response to thoracic vena cava constriction involves sympathetic efferent pathways, either by an intrarenal effect of circulatory catecholamines or by controlling the release of an extrarenal factor influencing sodium reabsorption.