Twenty-two patients with normal plasma renin and essential hypertension were classified as "salt-sensitive" (SS) (n = 9) or "non-salt-sensitive" (NSS) (n = 13) from an increase in mean blood pressure with changes in sodium intake from 25 to 250 meq/day. With the high sodium diet, the SS patients gained more weight (p less than 0.05), retained more sodium (p less than 0.05), and had a greater increase in cardiac output (p less than 0.05). Despite the markedly increased cardiac output, systemic vascular resistance did not change with sodium loads in the SS patients, whereas the NSS patients had a significant decrease in systemic vascular resistance. Thus, the greater increase in blood pressure with sodium loads in SS patients can be attributed not only to an increase in cardiac output, possibly resulting from greater sodium retention, but also to inappropriately elevated systemic vascular resistance. Concomitant with a greater increase in cardiac output, the SS patients had a greater increase in forearm blood flow with sodium loading than the NSS patients (p less than 0.02). In contrast, blood flow to the kidney and the liver was not significantly changed in either group; renal (p less than 0.05) and hepatic (p less than 0.01) vascular resistance increased significantly in SS patients but remained unchanged in NSS patients. Thus, evidence presented suggests that the greater increase in blood pressure with sodium loads seems to be characterized by a very inhomogenous 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 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.