Failure to demonstrate a humoral mechanism in the antinatriuresis of acute caval constriction.

Previous studies reported from this laboratory provided support for the hypothesis that the natriuresis of volume expansion is mediated in part by a humoral mechanism. In the present study we examined whether suppression of this factor participates in the antinatriuresis of acute constriction of the thoracic inferior vena cava. An isolated kidney was perfused by a second dog pretreated with deoxycorticosterone acetate. Expansion of the perfusion dog with equilibrated blood from a reservoir resulted in an increase in sodium excretion from 102+/-30 to 259+/-65 muEq/min, P < 0.001. Fractional sodium excretion increased from 2.3+/-0.6 to 6.2+/-1.2%, P < 0.01. Inulin clearance, plasma protein concentration, and packed cell volume remained constant; renal perfusion pressure and renal blood flow decreased. After the natriuresis was established, the thoracic inferior vena cava was constricted to decrease systemic arterial pressure in the perfusion dog 50 mm Hg. This maneuver suppressed urine output in the dog but did not significantly alter sodium excretion in the isolated kidney. During the period of caval constriction absolute sodium excretion in the isolated kidney measured 198+/-42 muEq/min and fractional sodium excretion measured 5.7+/-1.1%. Neither value is significantly different from that measured during volume expansion alone. The data suggest that the antinatriuresis of acute caval constriction probably does not require suppression of a humoral natriuretic factor and that other more rapidly acting mechanisms, presumably hemodynamic and neural, may be involved.