TY - JOUR
T1 - Cardiovascular actions of centrally and peripherally administered trout urotensin-I in the trout
AU - Mimassi, Nagi
AU - Shahbazi, Fatemeh
AU - Jensen, Jörgen
AU - Mabin, Dominique
AU - Conlon, J. Michael
AU - Le Mével, Jean Claude
PY - 2000
Y1 - 2000
N2 - 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. Intracerebro-ventricular 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 α-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 (pD2 = 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 neuro-hormone functioning either as a locally acting vasodilator or as a potent secretagogue of catecholamines.
AB - 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. Intracerebro-ventricular 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 α-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 (pD2 = 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 neuro-hormone functioning either as a locally acting vasodilator or as a potent secretagogue of catecholamines.
KW - Arterial blood pressure
KW - Cardiac output
KW - Catecholamines
KW - Heart rate
KW - Isolated vessels
KW - Teleost
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U2 - 10.1152/ajpregu.2000.279.2.r484
DO - 10.1152/ajpregu.2000.279.2.r484
M3 - Article
C2 - 10938236
AN - SCOPUS:0033858418
SN - 0363-6119
VL - 279
SP - R484-R491
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 2 48-2
ER -