Sodium-Selective Salt Sensitivity

Abstract

We tested the hypothesis that the Na + component of dietary NaCl can have a pressor effect apart from its capacity to complement the extracellular osmotic activity of Cl − and, thus, expand plasma volume. We studied 35 mostly normotensive blacks who ingested a low-NaCl diet, 30 mmol/d, for 3 weeks, in the first and third of which Na + was loaded orally with either NaHCO 3 or NaCl, in random order (250 mmol/d). In subjects adjudged to be salt sensitive (n=18; Δ mean arterial pressure: ≥5 mm Hg with NaCl load), but not in salt-resistant subjects (n=17), loading with NaHCO 3 was also pressor. The pressor effect of NaHCO 3 was half that of NaCl: mean arterial pressure (millimeters of mercury) increased significantly from 90 on low NaCl to 95 with NaHCO 3 and to 101 with NaCl. The pressor effect of NaCl strongly predicted that of NaHCO 3. As judged by hematocrit decrease, plasma volume expansion with NaCl was the same in salt-resistant and salt-sensitive subjects and twice that with NaHCO 3 , irrespective of the pressor effect. In salt-sensitive subjects, mean arterial pressure varied directly with plasma Na + concentration attained with all Na + loading. In salt-sensitive but not salt-resistant subjects, NaHCO 3 and NaCl induced decreases in renal blood flow and increases in renal vascular resistance; changes in renal blood flow were not different with the 2 salts. Responses of renal blood flow and renal vascular resistance to NaHCO 3 were strongly predicted by those to NaCl. In establishing the fact of “sodium-selective” salt sensitivity, the current observations demonstrate that the Na + component of NaCl can have pressor and renal vasoconstrictive properties apart from its capacity to complement Cl − in plasma volume expansion.