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Journal of Experimental Biology, Vol 202, Issue 8 1005-1013, Copyright © 1999 by Company of Biologists

JOURNAL ARTICLES

Vasodilation of swimbladder vessels in the european eel (Anguilla anguilla) induced by vasoactive intestinal polypeptide, nitric oxide, adenosine and protons

T Schwerte, S Holmgren and B Pelster
Institut fur Zoologie und Limnologie, Universitat Innsbruck, A-6020 Innsbruck, Austria and Department of Zoophysiology, University of Goteborg, Box 463, SE-40530 Goteborg, Sweden. Thorsten.Schwerte@uibk.ac.at.

The effects of &bgr;-adrenergic stimulation, vasoactive intestinal polypeptide (VIP), adenosine, the nitric oxide (NO)-releasing agent sodium nitroprusside and of metabolic end-products of gas gland cell metabolism on swimbladder blood flow were investigated using saline- or blood-perfused swimbladder preparations of the freshwater European eel Anguilla anguilla. While &bgr;-adrenergic vasodilation was not detectable, a bolus injection of adenosine (100 microl, 10(-)7 mol l-1) and application of VIP (10(-)7 mol kg-1) caused a significant decrease in perfusion pressure in saline-perfused swimbladder preparations. Immunohistochemical analysis revealed the presence of VIP-immunoreactive nerve fibres in the swimbladder artery and in the swimbladder vein (seawater-adapted eels were used for immunohistochemical studies). Application of sodium nitroprusside also elicited a small, but significant, decrease in perfusion pressure in saline-perfused swimbladder preparations, while preincubation of swimbladder tissue with N(&ohgr;)nitro-l-arginine, a non-selective inhibitor of nitric oxide synthase, significantly enhanced the flow-induced increase in perfusion pressure. Lactate, the major metabolic end-product of gas gland cell metabolism, had no effect on perfusion pressure. In contrast, an increase in proton concentration in both saline- and blood-perfused preparations induced a vasodilation, as indicated by a significant decrease in perfusion pressure. The results demonstrate that VIP, NO, adenosine and protons may induce a vasodilation of swimbladder blood vessels. None of these effects, however, compares in time span with the previously described immediate, short-lasting vasodilation of swimbladder vessels elicited by pulse stimulation of the vagus nerve.
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