Vasodilatory action of loop diuretics: a plethysmography study of endothelial function in forearm arteries and dorsal hand veins in hypertensive patients and controls.

Introduction: 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. Methods: 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. Results: 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. Conclusions: 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.