Cyclooxygenase inhibition restores nitric oxide activity in essential hypertension

Abstract

To evaluate whether cyclooxygenase constrictor substances can impair nitric oxide mediated vasodilation in essential hypertension, in seven normotensive subjects (43.3±4.1 years; BP, 117±6/81±2 mm Hg) and seven essential hypertensive patients (47.1±5.2 years; BP, 151±8/98±4 mm Hg) we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, 15 μg · 100 mL-1 · min-1) in basal conditions, during infusion of N(G)-monomethyl- L-arginine (L-NMMA; 100 μg · 100 mL-1 · min-1), a nitric oxide synthase inhibitor, or indomethacin (50 μg · 100 mL-1 · min-1), a cyclooxygenase inhibitor, or simultaneous indomethacin and L-NMMA. In normotensives, vasodilation to acetylcholine was blunted by L-NMMA (maximum flow increase: 671±64% and 386±42%, respectively; P