EFFECTS OF SEROTONIN ON THE CARDIO CIRCULATORY-SYSTEM OF THE EUROPEANEEL (ANGUILLA-ANGUILLA) IN-VIVO

Citation
Jj. Janvier et al., EFFECTS OF SEROTONIN ON THE CARDIO CIRCULATORY-SYSTEM OF THE EUROPEANEEL (ANGUILLA-ANGUILLA) IN-VIVO, Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology, 166(2), 1996, pp. 131-137
Citations number
28
Categorie Soggetti
Zoology,Physiology
ISSN journal
01741578
Volume
166
Issue
2
Year of publication
1996
Pages
131 - 137
Database
ISI
SICI code
0174-1578(1996)166:2<131:EOSOTC>2.0.ZU;2-U
Abstract
The effects of serotonin on continuously recorded cardiac parameters ( heart rate; cardiac output, cardiac stroke volume), ventral and dorsal aortic blood pressures, branchial and systemic vascular resistances w ere investigated in the European eel in vivo. Intravenous administrati on of serotonin (30 mu g . kg(-1)) caused a marked bradycardia (45%) a nd a simultaneous decrease in cardiac output (50%), ventral (35%) and dorsal (50%) aortic blood pressures. Branchial resistance was markedly increased (60%) and systemic resistance decreased (30%). Cardiac stro ke volume remained unchanged. The effects of serotonin on cardiac para meters were suppressed either by methysergide or a bilateral section o f the cardiac vagus. Bradycardia could then be regarded as the consequ ence of a vagal mechanism triggered by serotonin action on central met hysergide-sensitive serotonergic receptors. No inotropic effect of ser otonin was observed. This lack of myocardiac contractility modificatio n is discussed. The serotonin-mediated branchial vasoconstriction was attenuated by vagotomy, whereas the residual increase in branchial res istance (40%) was suppressed by methysergide. The serotonin-mediated b ranchial vasoconstriction could be the consequence of both a passive m echanism (compliance) caused by the decrease in cardiac output and an active mechanism involving methysergide-sensitive serotonergic recepto rs of the branchial vasculature. A possible involvement of this vasomo tor effect in gill oxygen uptake is discussed. The serotonin-induced s ystemic vasodilation was insensitive either to cardiac vagotomy or to 5-HT1/2, 5-HT3 and 5-HT4 receptor antagonists, suggesting the involvem ent of a local mechanism which remains to be assessed.