The effect of eprosartan on reflex sympathetic activation in sodium restricted
patients with essential hypertension.
Author(s): Vase H, Lauridsen TG, Graffe CC, Pedersen EB.
Affiliation(s): Department of Medical Research, Holstebro Hospital, Holstebro, Denmark.
henrikvase@dadlnet.dk
Publication date & source: 2011, J Am Soc Hypertens. , 5(5):385-94
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.
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