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First published online March 9, 2004
Journal of Experimental Biology 207, 1295-1303 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.00883

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Nitric oxide control of the dorsal aorta and the intestinal vein of the Australian short-finned eel Anguilla australis

Brett L. Jennings^*, Brad R. S. Broughton and John A. Donald

School of Biological and Chemical Sciences, Deakin University, Geelong, Victoria, Australia, 3217

^* Author for correspondence (e-mail: brettj{at}deakin.edu.au)

Accepted 19 January 2004

This study investigated the mechanisms by which nitric oxide (NO) regulates the dorsal aorta and the intestinal vein of the Australian short-finned eel Anguilla australis. NADPH diaphorase histochemistry and immunohistochemistry using a mammalian endothelial nitric oxide synthase (NOS) antibody could not demonstrate NOS in the endothelium of either blood vessel; however, NOS could be readily demonstrated in the endothelium of the rat aorta that was used as a control. Both blood vessels contained NADPH diaphorase positive nerve fibres and nerve bundles, and immunohistochemistry using a neural NOS antibody showed a similar distribution of neural NOS immunoreactivity in the perivascular nerves. In vitro organ bath physiology showed that a NO/soluble guanylyl cyclase (GC) system is present in the dorsal aorta and the intestinal vein, since the soluble GC inhibitor oxadiazole quinoxalin-1 (ODQ; 10^–5 mol l^–1) completely abolished the vasodilatory effect of the NO donor, sodium nitroprusside (SNP; 10^–4 mol l^–1). In addition, nicotine (3x10^–4 mol l^–1) mediated a vasodilation that was not affected by removal of the endothelium. The nicotine-mediated dilation was blocked by the NOS inhibitor, N-nitro-L-arginine (L-NNA; 10^–4 mol l^–1), and ODQ (10^–5 mol l^–1). More specifically, the neural NOS inhibitor, N-propyl-L-arginine (10^–5 mol l^–1), significantly decreased the dilation induced by nicotine (3x10^–4 mol l^–1). Furthermore, indomethacin (10^–5 mol l^–1) did not affect the nicotine-mediated dilation, suggesting that prostaglandins are not involved in the response. Finally, the calcium ionophore A23187 (3x10^–6 mol l^–1) caused an endothelium-dependent dilation that was abolished in the presence of indomethacin. We propose the absence of an endothelial NO system in eel vasculature and suggest that neurally derived NO contributes to the maintenance of vascular tone in this species. In addition, we suggest that prostaglandins may act as endothelially derived relaxing factors in A. australis.

Key words: nitric oxide, neural nitric oxide synthase, soluble guanylyl cyclase, vasodilation, nicotine, Anguilla australis, prostaglandin

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