Nerve-induced tachykinin-mediated vasodilatation in skeletal muscle is dependent on nitric oxide formation

Nerve-induced vasodilatation was studied by intravital microscopy of the rabbit tenuissimus muscle, pretreated with pancuronium, phentolamine, and guanethidine. Nerve stimulation of the tenuissimus nerve induced a vasodilatation which was frequency and pulse duration-dependent and insensitive to atr...

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Veröffentlicht in:European journal of pharmacology 1991-12, Vol.205 (3), p.295-301
Hauptverfasser: Persson, Magnus G., Hedqvist, Per, Gustafsson, Lars E.
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Sprache:eng
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Zusammenfassung:Nerve-induced vasodilatation was studied by intravital microscopy of the rabbit tenuissimus muscle, pretreated with pancuronium, phentolamine, and guanethidine. Nerve stimulation of the tenuissimus nerve induced a vasodilatation which was frequency and pulse duration-dependent and insensitive to atropine and propanolol but abolished by tetrodotoxin. The nitric oxide synthase inhibitor, N ω-nitro-L-arginine methyl ester (L-NAME, 100 μM), but not its enantiomer, D-NAME, markedly inhibited the vasodilatation induced by nerve stimulation or by exogenous substance P or neurokinin A. Vasodilatation due to calcitonin gene-related peptide, prostaglandin E 2 or nitroprusside was unaffected. The substance P antagonist, spantide (30 μM), significantly attenuated nerve-induced vasodilatation, in parallel with L-NAME Our results indicate that nerve-induced vasodilatation in skeletal muscle can be attributed to the release of substance P and/or other tachykinins and that nitric oxide subsequently mediates the response to endogenous tachykinins released from nerves.
ISSN:0014-2999
1879-0712
DOI:10.1016/0014-2999(91)90913-B