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. Attached Files Name Description MIMEType Size Downloads 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, 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 l−  1) 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 Collections: Faculty of Science, Engineering and Built Environment School of Life and Environmental Sciences Related Links Link Description Connect to published version (restricted access) Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Versions Version Filter Type Wed, 07 Jan 2009, 11:00:50 EST Wed, 15 Jul 2009, 10:10:24 EST Tue, 08 Sep 2009, 10:37:47 EST Mon, 16 Jun 2014, 09:07:48 EST Filtered Full Citation counts:   Cited 9 times in TR Web of Science Cited 9 times in Scopus Search Google Scholar Access Statistics: 1046 Abstract Views, 0 File Downloads  -  Detailed Statistics Created: Mon, 29 Sep 2008, 08:56:23 EST

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