Journal of cardiovascular pharmacology · 2007
Vasodilatory action of loop diuretics: a plethysmography study of endothelial function in forearm arteries and dorsal hand veins in hypertensive patients and controls.
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de Berrazueta José R, González Josefina Perez, de Mier Inmaculada, Poveda Jose J, García-Unzueta María-Teresa
Аннотация
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.
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.