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
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.