The Pathogenesis of Salt-Sensitive Hypertension

Abstract

Patients with normal plasma renin and essential hypertension can be divided into two groups according to blood pressure response to salt loading; salt-sensitive (SS) and non-salt-sensitive (NSS). With a high-sodium diet SS patients retained more sodium, and had a greater increase in cardiac output, as compared to NSS patients. Despite the markedly increased cardiac output, systemic vascular resistance did not change with sodium loads in the SS patients, suggesting inappropriately elevated systemic vascular resistance. The greater increase in blood pressure with sodium loads seems to be characterized by a very inhomogeneous distribution of local flow and resistance in SS patients; renal and hepatic blood flow remains essentially unchanged and skeletal muscle blood flow receives almost all of the increase in cardiac output. Moreover, systemic vascular resistance changes did not reflect the resistance of individual beds because vasoconstriction appeared in the kidney and in the splanchnic area but was masked by prominent vasodilation in the skeletal muscle. Because this hemodynamic pattern is similar to the pattern evoked during defense reaction, it is suggested that sympathetic overactivity on a selective basis might be involved in the impaired renal function for sodium excretion and the increase in blood pressure with sodium loads in SS patients.