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
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.