Cardiovascular actions of centrally and peripherally administered trout urotensin-I in the trout.

N Mimassi, F Shahbazi, J Jensen, D Mabin, J M Conlon, J C Le Mével

Index: Am. J. Physiol. Regul. Integr. Comp. Physiol. 279 , R484-R491, (2000)

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Abstract

The cardiovascular effects of centrally and peripherally administered synthetic trout urotensin (U)-I, a member of the corticotropin-releasing hormone family of neuroendocrine peptides, were investigated in unanesthetized rainbow trout Oncorhynchus mykiss. Intracerebroventricular injections of U-I (5.0 and 12.5 pmol) produced a sustained increase in mean dorsal aortic blood pressure (P(DA)) without significant change in heart rate (HR). This elevation in P(DA) was associated with an increase in cardiac output, but systemic vascular resistance did not change. Intra-arterial injection of U-I (12.5-500 pmol) evoked a dose-dependent increase in P(DA), but in contrast to the hemodynamic effects of centrally administered U-I, the hypertensive effect was associated with an increase in systemic vascular resistance and an initial fall in cardiac output. HR did not change or underwent a delayed increase. Pretreatment of trout with prazosin, an alpha-adrenoreceptor antagonist, completely abolished the rise in arterial blood pressure after intra-arterial administration of U-I, which was replaced by a sustained hypotension and tachycardia. Trout U-I produced a dose-dependent (pD(2) = 7.74 +/- 0.08) relaxation of preconstricted rings of isolated trout arterial vascular smooth muscle, suggesting that the primary action of the peptide in the periphery is vasorelaxation that is rapidly reversed by release of catecholamines. Our results suggest that U-I may regulate blood pressure in trout by acting centrally as a neurotransmitter and/or neuromodulator and peripherally as a neurohormone functioning either as a locally acting vasodilator or as a potent secretagogue of catecholamines.