Why the study?
Does volume expansion of a perfusion dog increase sodium excretion in an isolated kidney model?
Does volume expansion of a perfusion dog increase sodium excretion in an isolated kidney model?
Volume expansion in a perfusion dog induces natriuresis in an isolated kidney independent of physical or neurogenic factors, supporting the existence of a humoral natriuretic factor.
Supports humoral natriuretic factor in dogs; leaves open its identity, mechanism, and relevance to human sodium balance.
The role of a humoral mechanism in the natriuresis induced by volume expansion was evaluated using an isolated dog kidney perfused by a second dog which had been pretreated with desoxycorticosterone acetate (DOCA). Expansion of the perfusion dog with an equilibrated volume of blood from a reservoir, resulted in an increase in UnaV (sodium excretion) from 153.6+/-27.9 (sem) to 345.5+/-57.8 muEq/min, P<0.001. FEna (fractional sodium excretion) increased from 3.4+/-0.6 to 8.1+/-1.2%, P<0.01. The natriuresis occurred in the face of a significant decrease in Cin, RBF, and renal arterial pressure, and in the absence of any change in plasma protein concentration or packed cell volume. In a control group of experiments, sodium excretion did not change when the perfusion dog was not volume expanded, although Cin (inulin clearance) and RBF (renal blood flow) decreased to the same degree as in the expanded group. These data support the conclusion that volume expansion of the perfusion dog either stimulated the release of a natriuretic factor or suppressed the release of an antinatriuretic factor which was manifested by an increase in sodium excretion in the isolated kidney.
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Kaloyanides et al. (1971) studied this question.
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