Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/14287
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Type: Journal article
Title: Endogenous imidazoline receptor ligands relax rat aorta by an endothelium-dependent mechanism
Author: Musgrave, I.
van der Zypp, A.
Grigg, M.
Barrow, C.
Citation: Annals of the New York Academy of Sciences, 2003; 1009(1):222-227
Publisher: New York Acad Sciences
Issue Date: 2003
ISSN: 0077-8923
1749-6632
Editor: Piletz, J.E.
Regunathan, S.
Ernsberger, P.
Statement of
Responsibility: 
Ian F. Musgrave, Andrea Van Der Zypp, Mathew Grigg, Colin J. Barrow
Abstract: Agmatine and harmane have been proposed as endogenous ligands of imidazoline receptors. Agmatine has been reported to activate nitric oxide synthetase (NOS) in endothelial cells, so we sought to determine if agmatine or harmane and an analogue of harmane, propyl harmane, produced vasodilatation through an endothelium-dependent mechanism. The experiments were performed in endothelium-denuded and intact rat aortic rings preconstricted with phenylephrine (0.1 mM). Agmatine (0.3–1000 mM), harmane, and propyl harmane (0.3–100 mM) relaxed endothelium-intact rings in a concentration-dependent manner. Removal of endothelium inhibited the relaxant effect of agmatine, harmane, and propyl harmane. The NOS inhibitor L-NIO (100 mM) inhibited the relaxant effect of agmatine and harmane. The I₁-receptor antagonist AGN (100 mM) partly inhibited the effect of harmane but not that of agmatine. These results suggest that the endogenous imidazoline ligands are capable of stimulating NOS largely by an I₁-receptor-independent mechanism.
Keywords: agmatine
harmane
vasodilatation
nitric oxide
imidazoline receptors
Description: The definitive version is available at www.blackwell-synergy.com
DOI: 10.1196/annals.1304.027
Appears in Collections:Aurora harvest 2
Pharmacology publications

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