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EndothelinBreceptors are functionally important in mediating vasoconstriction in the systemic circulation in patients with left ventricular systolic dysfunction

By Peter J Cowburn, John G.F Cleland, John D McArthur, Margaret R MacLean, John J.V McMurray, Henry J Dargie and James J Morton

Abstract

AbstractOBJECTIVESThis study was designed to assess the functional importance of endothelin (ET)Breceptors in patients with left ventricular systolic dysfunction (LVSD) by comparing the hemodynamic effects of ET-1, a nonselective ETAand ETBagonist, with ET-3, a selective ETBreceptor agonist.BACKGROUNDKnowledge of the functional importance of ETBreceptors in mediating vasoconstriction in chronic heart failure will help determine whether antagonists at both ETAand ETBreceptors are required to fully prevent vasoconstriction to endogenously produced ET-1.METHODSWe infused ET-1 (5 and 15 pmol/min) and ET-3 (5 and 15 pmol/min) into two separate groups of eight patients with LVSD with similar baseline hemodynamic indices. Hemodynamics were measured using a pulmonary thermodilution catheter and an arterial line.RESULTSEndothelin-1 infusion led to systemic vasoconstriction, with a rise in mean arterial pressure (mean ± SEM 100 ± 3 to 105 ± 3 mm Hg, p < 0.02) and systemic vascular resistance (1,727 ± 142 to 2,055 ± 164 dyn/s/cm−5, p < 0.001) and a fall in cardiac index (2.44 ± 0.21 to 2.22 ± 0.20 liters/min/m2, p < 0.01). Endothelin-3 infusion also led to systemic vasoconstriction, with a rise in mean arterial pressure (99 ± 6 to 105 ± 6 mm Hg, p < 0.01) and systemic vascular resistance (1,639 ± 210 to 1,918 ± 245 dyn/s/cm−5, p < 0.01) and a fall in cardiac index (2.66 ± 0.28 to 2.42 ± 0.24 liters/min/m2, p < 0.05). Pulmonary hemodynamic measurements did not change significantly in either group.CONCLUSIONSBoth ET-1 and ET-3 infusions led to systemic vasoconstriction; the hemodynamic changes observed were of a similar magnitude at the same molar concentration. This suggests that ETBreceptors are functionally important in mediating vasoconstriction, at least in the systemic circulation, in patients with LVSD

Publisher: American College of Cardiology. Published by Elsevier Inc.
Year: 1999
DOI identifier: 10.1016/S0735-1097(98)00663-9
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