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Mechanisms of vasodilation in the dorsal aorta of the elephant fish, Callorhinchus milii (Chimaeriformes: Holocephali)

Jennings, Brett L., Bell, Justin D., Hyodo, Susumu, Toop, Tes and Donald, John 2007, Mechanisms of vasodilation in the dorsal aorta of the elephant fish, Callorhinchus milii (Chimaeriformes: Holocephali), Journal of comparative physiology B, vol. 177, no. 5, pp. 557-567, doi: 10.1007/s00360-007-0154-7.

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Title Mechanisms of vasodilation in the dorsal aorta of the elephant fish, Callorhinchus milii (Chimaeriformes: Holocephali)
Formatted title Mechanisms of vasodilation in the dorsal aorta of the elephant fish, Callorhinchus milii (Chimaeriformes: Holocephali)
Author(s) Jennings, Brett L.
Bell, Justin D.
Hyodo, Susumu
Toop, Tes
Donald, JohnORCID iD for Donald, John orcid.org/0000-0001-5930-2642
Journal name Journal of comparative physiology B
Volume number 177
Issue number 5
Start page 557
End page 567
Publisher Springer
Place of publication Heidelberg, Germany
Publication date 2007-07
ISSN 0174-1578
1432-136X
Keyword(s) holocephalan
calcitonin gene-related peptide
prostaglandin
nitric oxide
vasodilation
nitric oxide synthase
Summary This study investigated vasodilator mechanisms in the dorsal aorta of the elephant fish, Callorhinchus milii, using anatomical and physiological approaches. Nitric oxide synthase could only be located in the perivascular nerve fibres and not the endothelium of the dorsal aorta, using NADPH histochemistry and immunohistochemistry. In vitro organ bath experiments demonstrated that a NO/soluble guanylyl cyclase (GC) system appeared to be absent in the vascular smooth muscle, since the NO donors SNP (10−4 mol l−1) and SIN-1 (10−5 mol l−1) were without effect. Nicotine (3 × 10−4 mol l−1) mediated a vasodilation that was not affected by ODQ (10−5 mol l−1), l-NNA (10−4 mol l−1), indomethacin (10−5 mol l−1), or removal of the endothelium. In contrast, the voltage-gated sodium channel inhibitor, tetrodotoxin (10−5 mol l−1), significantly decreased the dilation induced by nicotine, suggesting that it contained a neural component. Pre-incubation of the dorsal aorta with the calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP8–37 (10−6 mol l1) also caused a significant decrease in the nicotine-induced dilation. We propose that nicotine is mediating a neurally-derived vasodilation in the dorsal aorta that is independent of NO, prostaglandins and the endothelium, and partly mediated by CGRP.
Language eng
DOI 10.1007/s00360-007-0154-7
Field of Research 060603 Animal Physiology - Systems
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2007, Springer
Persistent URL http://hdl.handle.net/10536/DRO/DU:30007813

Document type: Journal Article
Collection: School of Life and Environmental Sciences
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