Factors involved in antinatriuretic effects of acute constriction of the thoracic and abdominal inferior vena cava.

Abstract

Studies were performed on anesthetized saline-loaded dogs to delineate the factors involved in the antinatriuretic effect of acute constriction of the thoracic (TIVC) and abdominal (AIVC) inferior vena cava. Acute TIVC constriction lowered cardiac output and arterial blood pressure and reduced urinary sodium excretion 48%; the same degree of reduction in renal perfusion pressure by suprarenal aortic constriction diminished sodium excretion only 27%. This finding suggested that factors other than a reduction in renal perfusion pressure are involved in the antinatriuretic effect of acute TIVC constriction. This conclusion was confirmed by studies in which a significant antinatriuretic effect (23%) was observed during acute TIVC constriction while renal perfusion pressure and renal venous pressure were held constant. A similar degree of constriction of the AIVC, as judged by the increase in vena cava pressure, did not cause a decrease in arterial pressure or cardiac output, and the modest antinatriuretic effect of this maneuver was not observed when renal venous pressure was held constant. The antinatriuretic effect of TIVC constriction which occurred in the absence of changes in renal perfusion pressure and renal venous pressure did not correlate with alterations in renal vascular resistance, glomerular filtration rate, and calculated initial postglomerular protein concentration and was not abolished by renal denervation or adrenalectomy. The afferent stimulus for the antinatriuretic effect may be related to the alterations in systemic hemodynamics which occur during acute TIVC, but not AIVC, constriction.