Exaggerated natriuresis in salt-sensitive essential hypertension.

Acute responses of blood pressure and natriuresis to intravenous injection of furosemide and saline infusion were evaluated in 38 patients with essential hypertension. Twelve patients whose mean arterial blood pressure decreased by more than 5% at two hours after intravenous administration of 20 mg furosemide were classified as salt-sensitive (SS); the remainders as salt-resistant (SR). The extent of natriuresis induced by furosemide was not different between the two subgroups. During 2-liter isotonic saline infusion the SS subjects excreted more sodium than the SR subjects did (108.7 +/- 11.9 vs 55.9 +/- 6.6 mmole, p less than 0.001). There was a significant correlation (r = 0.57, p less than 0.001) between the hypotensive effect of furosemide and the 4-hour sodium excretion during saline infusion. A reverse correlation between the sodium excretion during saline infusion and the increase in mean blood pressure at the end of infusion was shown in the SS subgroup (r = -0.72, p less than 0.01), but not in the SR subgroup (r = 0.045). The results suggest that prompt natriuresis on saline infusion in the SS hypertensives may function as a protective mechanism to prevent abrupt increase in blood volume and blood pressure during acute sodium loading.