The effect of eprosartan on reflex sympathetic activation in sodium restricted patients with essential hypertension.

AT(1) receptor antagonists possess sympathoinhibitory effects in animal experiments, but in human studies the results are conflicting. We tested the hypothesis that very short-term treatment with the AT(1) receptor antagonist eprosartan inhibits reflex activation of the sympathetic nervous system in sodium-restricted patients with essential hypertension. The effect of eprosartan on urinary sodium and lithium excretion, heart rate, blood pressure, and vasoactive hormones was measured during reflex activation of the sympathetic nervous system by a cold pressor test and by a sodium nitroprusside induced 10 mm Hg reduction of the mean arterial pressure. It was a randomized, placebo-controlled, double-blinded, crossover study in 14 patients with essential hypertension. Glomerular filtration rate and renal tubular function were determined with continuous infusion clearance technique and vasoactive hormones with radioimmunoassays. Eprosartan had no effect on the increases in heart rate and plasma levels of noradrenaline during reflex activation of the sympathetic nervous system. However, eprosartan significantly decreased in fractional excretions of sodium (mean ± SD) (0.23 ± 0.22%) and lithium (3.1 ± 1.7%) during the sodium nitroprusside infusion, compared to placebo. Very short-term eprosartan treatment does not seem to have any sympathoinhibitory effects in sodium restricted patients with essential hypertension.