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

Jennings, Brett L., Broughton, Brad R. S. and Donald, John 2004, Nitric oxide control of the dorsal aorta and the intestinal vein of the Australian short-finned eel Anguilla australis, Journal of experimental biology, vol. 207, pp. 1295-1303, doi: 10.1242/jeb.00883.

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Title Nitric oxide control of the dorsal aorta and the intestinal vein of the Australian short-finned eel Anguilla australis
Author(s) Jennings, Brett L.
Broughton, Brad R. S.
Donald, JohnORCID iD for Donald, John orcid.org/0000-0001-5930-2642
Journal name Journal of experimental biology
Volume number 207
Start page 1295
End page 1303
Publisher Company of Biologists
Place of publication Cambridge, England
Publication date 2004
ISSN 0022-0949
1477-9145
Keyword(s) nitric oxide
neural nitric oxide synthase
soluble guanylyl cyclase
vasodilation
nicotine
Anguilla australis
prostaglandin
Summary 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, Nω-nitro-arginine (L-NNA; 10–4 mol l–1), and ODQ (10–5 mol l–1). More specifically, the neural NOS inhibitor, Nω-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.
Notes First published online March 9, 2004
Language eng
DOI 10.1242/jeb.00883
Field of Research 060603 Animal Physiology - Systems
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2004, Company of Biologists
Persistent URL http://hdl.handle.net/10536/DRO/DU:30002712

Document type: Journal Article
Collection: School of Biological and Chemical Sciences
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