AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 3 771-R778, Copyright © 1995 by American Physiological Society
Responses of the branchial circulation to hypoxia in the Atlantic cod, Gadus morhua
L. I. Sundin
Department of Zoophysiology, University of Goteborg, Sweden.
Simultaneous measurements of ventral aortic pressure, dorsal aortic
pressure, cardiac output, and branchial venous flow were made to assess the
effects of external hypoxia on the branchial vasculature in vivo. In
addition, the effects of exogenously added amines (epinephrine and
serotonin) and their antagonists (prazosin, sotalol, and methysergide) were
assessed. The net effect of hypoxia was to increase branchial venous flow.
Mechanisms involved in the branchial vasomotor control include an
alpha-adrenoceptor-mediated vasoconstriction, as well as a nonadrenergic,
possibly serotonergic, vasodilation of the arteriovenous pathway. The
arterioarterial vascular resistance remained largely constant during
hypoxia: a beta-adrenoceptor vasodilator effect was offset by
vasoconstrictor factors that could be unmasked by sotalol treatment. One of
these arterioarterial vasoconstrictors may be serotonin (released from
serotonergic nerves or neuroepithelial cells), acting on the efferent
filamental artery sphincters. The vascular adjustments during hypoxia
increased the portion of cardiac output that flowed to the arteriovenous
pathway. This may be of importance in providing the heart and the
ion-regulatory cells of the filamental epithelium with oxygenated blood.
