P-166: Selective sodium-loading induces renal vasoconstriction in salt-sensitive african-americans

We recently reported that sodium-loading with NaHCO3, as well as NaCl, can induce a robust pressor effect in salt-sensitive (SS) but not in salt-resistant (SR) African-Americans with normal or mildly elevated blood pressures. As judged by the change in hematocrit, expansion of plasma volume (PV) was twice that with NaCl than with equimolar NaHCO3, but similar in SS and SR. These observations suggest that a) sodium per se can be a pressor agent and b) PV expansion may be necessary but not sufficient for the pressor response to sodium-loading. The pathophysiologic mechanism of salt-sensitivity may involve a dysfunctional renal hemodynamic response to increased dietary NaCl: with NaCl-loading, renal vascular resistance (RVR) has been shown to increase and renal blood flow (RBF) to either decrease or fail to increase. Thus, the pressor effect of NaCl may be mediated by renal vasoconstrictive dysfunction induced by the sodium-component of NaCl. To test this hypothesis, we measured RBF and RVR in 16 SS and 15 SR African Americans with normal or mildly elevated blood pressures who ingested a low NaCl-diet, 30 mmol/d, for three sequential 7-day periods, in the first and third of which sodium was loaded orally with either NaHCO3 or NaCl, in random order, 250 mmol/d. In SS but not SR, NaHCO3 as well as NaCl induced a significant decrease in RBF and increase in RVR. In SS, RBF (ml/min/1.73m2; mean and 95% C.I.) decreased from 965 (132) on the low NaCl-diet to 868 (114) with NaHCO3, p