Vasodilatory Action of Loop Diuretics: A Plethysmography Study of Endothelial Function in Forearm Arteries and Dorsal Hand Veins in Hypertensive Patients and Controls

Abstract

Intravenous administration of loop diuretics induces venodilation before the diuretic response. We investigated whether furosemide and torasemide exert a dilatory effect on arteries and veins mediated by endothelial release of nitric oxide. We performed intermittent venous occlusion plethysmography to study forearm blood flow and dorsal hand-vein distension in response to furosemide and torasemide infusion in hypertensive patients and healthy controls. Furosemide increased venodilation from 0.56 +/- 0.09 to 0.88 +/- 0.06 (P=0.000) in control subjects and from 0.49 +/- 0.10 to 0.75 +/- 0.12 (P=0.000) in hypertensive patients. Torasemide increased venodilation from 0.46 +/- 0.06 to 0.70 +/- 0.11 (P=0.007) in control subjects and from 0.48 +/- 0.09 to 0.67 +/- 0.12 (P = 0.03) in hypertensive patients. Co-infusion of the Nitric Oxide Synthase Inhibitor (L-NMMA)-blocked this venodilation, and the action was reversed with L-arginine. There were no significant changes in the arterial bed. Furosemide and torasemide induce a similar dose-response curve venodilation, but they have no effect on the arterial bed. Hypertensive patients show a smaller venous endothelium-dependent response than healthy controls. The venodilation induced by both diuretics requires release of nitric oxide.