Volume expansion inhibits renal nerve activity primarily through cardiopulmonary receptors with afferent vagal fibers rather than sinoaortic baroreceptors.
Should not change clinical volume management; leaves open translation of cardiopulmonary vagal dominance to human cardiorenal states.
Volume expansion could inhibit renal nerve activity by stimulating cardiopulmonary baroreflexes or by increasing arterial pressure (i.e., stimulating the sinoaortic baroreflexes). Our study assessed the relative roles of these two reflexes in the renal nerve activity responses to volume expansion (15 ml/kg 6% dextran in normal saline). With cardiopulmonary and arterial baroreflexes intact, volume expansion resulted in increases in arterial pressure and pulmonary artery wedge pressure and in decreases in renal nerve activity. After sinoaortic denervation, volume expansion resulted in similar decreases in renal nerve activity for similar increases in pulmonary artery wedge pressure. In contrast, after selective vagotomy (sinoaortic baroreflexes intact) volume expansion resulted in increases in arterial pressure and pulmonary artery wedge pressure, but reductions in renal nerve activity were markedly attenuated. After sinoaortic denervation and vagotomy, volume expansion did not result in significant changes in renal nerve activity. We conclude that decreases in renal nerve activity during volume expansion are mediated mainly by cardiopulmonary receptors with afferent vagal fibers. Sinoaortic baroreceptors appear to play a minor role in mediating these responses.
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Thames et al. (1982) studied this question.
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