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Laboratoire de Neurophysiologie, Unité de Formation et de Recherche de Médecine, Université de Bretagne Occidentale, 29285 Brest Cedex, and European Institute for Peptide Research, Laboratory of Cellular and Molecular Neuroendocrinology, Institut National de la Santé et de la Recherche Médicale U-413, Unité Associée au Centre National de la Recherche Scientifique, University of Rouen, 76821 Mont-Saint-Aignan, France
The
central and peripheral cardiovascular effects of endothelin (ET)-1 and
ET-3 were investigated in conscious rainbow trout. Both
intracerebroventricular and intra-arterial injections of ET-1
(6.25-25 pmol) but not ET-3 (25 pmol) caused a dose-dependent increase in mean dorsal aortic blood pressure and a concomitant decrease in heart rate. The hypertensive effects induced by
intra-arterial and intracerebroventricular injection of ET-1 were
associated with a significant (P < 0.05) increase in systemic vascular resistance. Intracerebroventricular
injection of ET-1 induced a twofold higher pressor response than that
caused by intra-arterial injection of ET-1 and provoked a barostatic
gain that was reduced by 2.5- to 3-fold compared with that calculated
after intra-arterial administration of the peptide. The ET receptor
antagonist bosentan significantly (P < 0.05) attenuated these responses regardless of the route of
administration. Finally, intra-arterial injection of ET-1 did not
significantly modify plasma cortisol level. The present data demonstrate that intracerebroventricular and intra-arterial
administration of very low doses of ET-1 produces hypertension in
conscious trout. The lack of effect of ET-3 indicates that the
hemodynamic actions of ET-1 are mediated both centrally and
peripherally through ETA receptors.
bosentan; arterial blood pressure; heart rate; cardiac output
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