CARDIOVASCULAR ACTIONS OF TROUT UROTENSIN-II IN THE CONSCIOUS TROUT, ONCORHYNCHUS-MYKISS

Citation
Jc. Lemevel et al., CARDIOVASCULAR ACTIONS OF TROUT UROTENSIN-II IN THE CONSCIOUS TROUT, ONCORHYNCHUS-MYKISS, American journal of physiology. Regulatory, integrative and comparative physiology, 40(5), 1996, pp. 1335-1343
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
40
Issue
5
Year of publication
1996
Pages
1335 - 1343
Database
ISI
SICI code
0363-6119(1996)40:5<1335:CAOTUI>2.0.ZU;2-E
Abstract
The central and peripheral cardiovascular effects of synthetic trout u rotensin II (UII) were investigated in the conscious rainbow trout. In tracerebroventricular 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 icy produced a significant (P < 0.05) rise (8%) in blood pressure with no change in heart rate. In contrast to the weak presser effect of centrally admin istered UII, intra-arterial injection of UII produced a dose-dependent increase in arterial blood pressure and decrease in heart rate with s ignificant (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 p ressure, was abolished by pretreatment with phentolamine. Trout UII pr oduced a sustained and dose-dependent contraction of isolated vascular rings prepared from trout efferent branchial [-log 50% of the concent ration producing maximal contraction (pD(2)) = 8.30] and celiacomesent eric (pD(2) = 8.22) arteries but was without effects on vascular rings from the anterior cardinal vein. The data indicate that the presser e ffect of UII in trout is mediated predominantly, if not exclusively, b y an increase in systemic vascular resistance. The UII-induced hyperte nsive response does not seem to involve release of catecholamines, but the bradycardia may arise from adrenergic-mediated activation of card ioinhibitory baroreflexes.