What Initiates the Pressor Effect of Salt in Salt-Sensitive Humans? Observations in Normotensive African Americans

We tested the traditional hypothesis that an abnormally enhanced renal reclamation of dietary NaCl alone initiates its pressor effect (“salt-sensitivity”). Under metabolically controlled conditions, we grouped 23 normotensive African Americans as either salt-sensitive (SS) or salt-resistant (SR), depending on whether or not dietary NaCl-loading did or did not increase mean arterial blood pressure (MAP) by ≥ 5mmHg. We determined whether dietary NaCl-loading induces: a) greater increases in external Na + balance, plasma volume and cardiac output (CO) in SS, compared to any in SR; and b) differential changes in systemic vascular resistance (SVR) that could account for the pressor differences between SS and SR. Using impedance cardiography, we measured CO and SVR daily at 4-hr intervals throughout the last 3 days of a 7-day period of low NaCl intake, 30mmol/d, and throughout a subsequent 7-day period of NaCl-loading, 250mmol/d. In the 11 SS, compared to the 12 SR, NaCl-loading induced no greater increases in Na + balance, body weight, plasma volume and CO. Yet, from days 2 to 7 of NaCl-loading, changes of MAP in SS diverged progressively from those in SR. From days 2 to 4, progressive increases of MAP in SS reflected importantly impaired decreases of SVR, as judged from “normal” decreases of SVR in SR. In SS and SR combined, changes in both MAP and SVR on day 2 strongly predicted changes in MAP on day 7. In many normotensive African Americans, vascular dysfunction is critical to the initiation of a pressor response to dietary NaCl.