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First published online September 16, 2005
Journal of Experimental Biology 208, 3739-3746 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01834

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Endothelin-1 causes systemic vasodilatation in anaesthetised turtles (Trachemys scripta) through activation of ET_B-receptors

Nini Skovgaard^1,*, Daniel E. Warren^1,2, Donald C. Jackson² and Tobias Wang¹

¹ Department of Zoophysiology, Institute of Biological Sciences, University of Aarhus, Denmark
² Department of Molecular Pharmacology, Physiology and Biotechnology, Brown University, Providence, RI 02912, USA

^* Author for correspondence (e-mail: nini.jensen{at}biology.au.dk)

Accepted 15 August 2005

The effects of endothelin-1 (ET-1) on systemic and pulmonary circulation were investigated in anaesthetised freshwater turtles (Trachemys scripta) instrumented with arterial catheters and blood flow probes. Bolus intra-arterial injections of ET-1 (0.4–400 pmol kg^-1) caused a dose-dependent systemic vasodilatation that was associated with a decrease in systemic pressure (P_sys) and a rise in systemic blood flow (_sys), causing systemic conductance (G_sys) to increase. ET-1 had no significant effects on the pulmonary vasculature, heart rate (fH) or total stroke volume (VS_tot). This response differs markedly from mammals, where ET-1 causes an initial vasodilatation that is followed by a pronounced pressor response. In mammals, the initial dilatation is caused by stimulation of ET_B-receptors, while the subsequent constriction is mediated by ET_A-receptors. In the turtles, infusion of the ET_B-receptor agonist BQ-3020 (150 pmol kg^-1) elicited haemodynamic changes that were similar to those of ET-1, and the effects of ET-1 were not affected by the ET_A-antagonist BQ-610 (0.15 µmol kg^-1). Conversely, all effects of ET-1 were virtually abolished after specific ET_B-receptor blockade with the ET_B-antagonist BQ-788 (0.15 µmol kg^-1). The subsequent treatment with the general ET-receptor antagonist tezosentan (15.4 µmol kg^-1) did not produce effects that differed from the treatment with ET_B-antagonist, and the blockade of ET-1 responses persisted. This present study indicates, therefore, that ET_B-receptors are responsible for the majority of the cardiovascular responses to ET-1 in Trachemys.

Key words: turtle, Trachemys, reptile, blood flow, blood pressure, systemic circulation, pulmonary circulation, endothelin, ET_A-receptor, ET_B-receptor

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