Endothelium-independent constriction of isolated, pressurized arterioles by N-omega nitro-L-arginine methyl ester (L- NAME)

Murphy, T, Kotecha, N and Hill, M 2007, 'Endothelium-independent constriction of isolated, pressurized arterioles by N-omega nitro-L-arginine methyl ester (L- NAME)', British Journal of Pharmacology, vol. 151, no. 5, pp. 602-609.


Document type: Journal Article
Collection: Journal Articles

Title Endothelium-independent constriction of isolated, pressurized arterioles by N-omega nitro-L-arginine methyl ester (L- NAME)
Author(s) Murphy, T
Kotecha, N
Hill, M
Year 2007
Journal name British Journal of Pharmacology
Volume number 151
Issue number 5
Start page 602
End page 609
Total pages 8
Publisher Nature Publishing Group
Abstract BACKGROUND & PURPOSE - Nitric oxide synthase (NOS) inhibitors cause vasoconstriction in pressurized arterioles with myogenic tone. This suggests either tonic production of NO modulates myogenic tone or a direct, NOS-independent effect of the NOS inhibitors. The nature of the contractile effect of the nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME, 100 mu M) on pressurised arterioles was investigated. EXPERIMENTAL APPROACH - Segments of rat cremaster muscle first- order arteriole were cannulated on glass micropipettes and maintained at an intraluminal pressure of 50, 70 or 120 mmHg. Key results: L-NAME and the related compound L-NA (100 mM) constricted pressurized vessels with myogenic tone. Removal of the endothelium did not cause constriction or alter myogenic tone, however the constrictor effect of L-NAME persisted. The constrictor effect of L-NAME was abolished by L-arginine (1 mM). Other NO and cGMP pathway inhibitors, including the nNOS inhibitor 7-nitroindazole (100 mM), the NO scavenger carboxy-PTIO (100 mM), the guanylate cyclase inhibitor ODQ (10 mM) and the cGMP inhibitor Rp-8CPT-cGMPS (10 mM) did not cause constriction of the arterioles. L-NAME caused a small (3-4 mV) but not statistically significant depolarization of the arteriolar smooth muscle at both pressures. The constrictor effect was not prevented by the K+ channel antagonist tetraethyl ammonium (TEA, 1 mM) or the K-ATP channel antagonist glibenclamide (1 mM). CONCLUSIONS & IMPLICATIONS - These observations demonstrate that L-NAME causes an endothelium- and NOS-independent contraction of vascular smooth muscle in isolated skeletal muscle arterioles. It is suggested that the underlying mechanism relates to an arginine binding interaction.
Subject Basic Pharmacology
Keyword(s) Skeletal-Muscle Arterioles
Smooth-Muscle
Myogenic Tone
Dependent Mechanisms
Resistance Arteries
Potassium Channels
Cerebral-Artery
Rat
Responses
Oxide
Copyright notice © 2007 Nature Publishing Group
ISSN 0007-1188
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