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Am J Physiol Regul Integr Comp Physiol 271: R1335-R1343, 1996;
0363-6119/96 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 271, Issue 5 1335-R1343, Copyright © 1996 by American Physiological Society


ARTICLES

Cardiovascular actions of trout urotensin II in the conscious trout, Oncorhynchus mykiss

J. C. Le Mevel, K. R. Olson, D. Conklin, D. Waugh, D. D. Smith, H. Vaudry and J. M. Conlon
Laboratoire de Neurophysiologie, Universite de Bretagne Occidentale, Brest, France.

The central and peripheral cardiovascular effects of synthetic trout urotensin II (UII) were investigated in the conscious rainbow trout. Intracerebroventricular injection of 50 pmol UII produced a slight (3%) but significant (P < 0.05) increase in heart rate but had no effect on mean arterial blood pressure. Injection of 500 pmol UII icv produced a significant (P < 0.05) rise (8%) in blood pressure with no change in heart rate. In contrast to the weak pressor effect of centrally administered UII, intra-arterial injection of UII produced a dose-dependent increase in arterial blood pressure and decrease in heart rate with significant (P < 0.05) effects on both parameters observed at a dose of 25 pmol. Higher doses of the peptide produced a sustained decrease in cardiac output that accompanied the bradycardia and rise in arterial blood pressure. The UII-induced bradycardia, but not the increase in pressure, was abolished by pretreatment with phentolamine. Trout UII produced a sustained and dose-dependent contraction of isolated vascular rings prepared from trout efferent branchial [-log 50% of the concentration producing maximal contraction (pD2) = 8.30] and celiacomesenteric (pD2 = 8.22) arteries but was without effects on vascular rings from the anterior cardinal vein. The data indicate that the pressor effect of UII in trout is mediated predominantly, if not exclusively, by an increase in systemic vascular resistance. The UII-induced hypertensive response does not seem to involve release of catecholamines, but the bradycardia may arise from adrenergic-mediated activation of cardioinhibitory baroreflexes.


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