We recently reported that when dietary potassium was controlled at a marginally deficient intake not uncommon in many African- Americans (blacks), 30 mmol/d, salt sensitivity occurred in the majority of normotensive blacks but in relatively few normotensive Caucasian-Americans (whites), and on average was more severe in blacks. In a subsequent study of normotensive and mildly hypertensive black men consuming a diet marginally deficient in potassium, we observed that in those who were salt- sensitive, dietary NaCl loading induced a renal vasoconstrictive dysfunction in which renal blood flow (RBF) decreased, renal vascular resistance (RVR) and filtration (FF) increased, and glomerular filtration rate trended upward. The changes in mean arterial pressure induced by dietary NaCl varied inversely with those induced in RBF and directly with those in RVR and FF. In those blacks who were not salt-sensitive, renal dysfunction was not observed with NaCl loading. Since dietary loading of sodium citrate (and other non-Cl sodium salts) fails to induce a pressor response in patients with salt-sensitive hypertension, sodium citrate might also fail to induce a renal vasoconstrictive dysfunction in normotensive salt-sensitive blacks. We anticipate this finding, and will interpret it as evidence suggesting that the pressor effect induced in blacks by NaCl loading requires the induction of a renal vasoconstrictive dysfunction, which in turn requires the Cl- component of loaded NaCl. We have recently reported that in the stroke-prone spontaneously hypertensive rat fed a normal NaCl diet, supplemental KCl induced a persisting exacerbation of hypertension, renal vasculopathy and strokes, whereas supplemental KHCO3 had opposite effects. When this rat was NaCl-loaded, supplemental KCl, but not KHCO3, further exacerbated hypertension and the renal vasculopathy, increased the frequency of strokes, and within hours induced a reduction in urinary creatinine excretion. In normotensive and mildly hypertensive blacks fed a normal NaCl diet (150mmol/d) just adequate in potassium (45 mmol/d), we will determine whether KCl and K-citrate (100 mmol/d) supplemented for 14 days have differing pressor and renal hemodynamic effects. We anticipate that both supplemented potassium salts will induce a decrease in blood pressure, but that a lower RBF and a higher RVR and FF will attend supplemental KCl. We will interpret such findings as suggesting that the Cl component of KCl can exert a renal vasoconstrictive and potentially renopathic effect despite a concomitant decrease in blood pressure.
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