Eighteen patients with hypertension in whom all known causes of elevated blood pressure levels had been ruled out were studied during a low-sodium diet for seven days, a high-sodium diet for seven days and after the oral administration of furosemide. They were classified as “salt-sensitive” (SS) or “nonsalt-sensitive” (NSS) from the increase in 24-hour averages of mean blood pressure with changes in sodium intake from 9 meq to 249 meq/day (15.1 ± 1.2 (SE) mm Hg (SS) versus 2.7 ± 0.9 mm Hg (NSS), (p < 0.001)). With a highsodium diet, SS patients gained more weight (p < 0.001), retained more sodium (p < 0.05), had a greater increase in cardiac output (p < 0.05), showed higher plasma norepinephrine levels on day 4 (p < 0.05), showed lesser decrements in PRA and plasma aldosterone concentration than the NSS patients, and showed no change in urinary prostaglandin E2 (PGE2) which decreased (p < 0.01) in the NSS patients. With furosemide, SS patients showed greater decrements in cardiac output (p < 0.05) and showed no change in urinary PGE2, whereas NSS patients showed increases (p < 0.01). Results suggest that the greater increase in blood pressure in SS patients with sodium loading can be attributed to greater sodium retention, leading in turn to an increase in cardiac output. The persistence of autonomic “drive” in the SS patients may contribute to the relative sodium retention with sodium loads and the increase in blood pressure.

Factors influencing blood pressure in salt-sensitive patients with hypertension