Furosemide is a loop diuretic that inhibits the Na-K-2Cl symporter in the loop of Henle. It exerts direct vasoactive effects, as well as hormonally mediated changes via release of renin, angiotensin II, and prostaglandins. These result in arterial vasoconstriction and venous vasodilation, as well as diuresis.
In heart failure patients, it has been demonstrated that venous capacitance and blood flow in the calf increased within 5 minutes after administration of furosemide, an effect that preceded diuresis by 25 minutes, indicating direct venodilatory effects. It was also noted that there was a reduction in right atrial pressure and PCWP, indicating an acute reduction in preload that was not attributable to diuretic effects of furosemide. Therefore, the acute venodilatory effects of furosemide may be a larger contributor in the early clinical improvement of acute heart failure symptoms than diuresis. This direct venodilatory effect of furosemide may be mediated by local vascular prostaglandin synthesis.
References
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- P Pickkers, T P Dormans, F G Russel, A D Hughes, T Thien, N Schaper, P Smits Direct vascular effects of furosemide in humans. Circulation: 1997, 96(6);1847-52 PubMed Link
- P S Jhund, J J McMurray, A P Davie The acute vascular effects of frusemide in heart failure. Br J Clin Pharmacol: 2000, 50(1);9-13 PubMed Link
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