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Vasodilator mechanisms in intermediate‐ and small‐sized arteries from the toad, Bufo marinus (879.10)
Author(s) -
Cameron Melissa,
Donald John
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.879.10
Subject(s) - vasodilation , nitric oxide , endothelium , acetylcholine , vasoconstriction , medicine , myograph , nitric oxide synthase , anatomy , chemistry , endocrinology , pharmacology , cardiology
Nitric oxide (NO), prostaglandins (PG) and endothelium‐derived hyperpolarising factor/s (EDHF) released by the endothelium are mediators of vasodilation in intermediate‐ and small‐sized resistance arteries of mammals. In this study, small vessel myography was used to determine the vasodilator mechanisms in the intermediate‐sized iliac artery and the small‐sized gastrocnemius artery of toad. Acetylcholine (ACh) was used to activate signalling systems that mediate vasodilation. In the iliac artery, ACh vasodilation was abolished by blockade of the NO and PG signalling pathways with ODQ and indomethacin, respectively. Furthermore, removal of the endothelium had no effect on the ACh vasodilation in the iliac artery. In contrast, ACh vasodilation in the gastrocnemius artery included NO and PG components, but there was a third endothelium‐dependent component that could be due to an EDHF, as the ACh dose‐response curve was shifted to the right by the K channel antagonist, TEA. Thus, the mechanisms of vasodilation in the amphibian arterial tree are dependent on the size of the vessel, and the endothelium may become more important as vessel size diminishes. This is the first time this has been shown in a non‐mammalian vertebrate in which the endothelial cells do not express an endothelial nitric oxide synthase.