Persson M G, Hedqvist P, Gustafsson L E
Department of Physiology, Karolinska Institutet, Stockholm, Sweden.
Eur J Pharmacol. 1991 Dec 3;205(3):295-301. doi: 10.1016/0014-2999(91)90913-b.
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 omega-nitro-L-arginine methyl ester (L-NAME, 100 microM), but not its enantiomer, D-NAME, markedly inhibited the vasodilation induced by nerve stimulation or by exogenous substance P or neurokinin A. Vasodilatation due to calcitonin gene-related peptide, prostaglandin E2 or nitroprusside was unaffected. The substance P antagonist, spantide (30 microM), 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.
通过对预先用泮库溴铵、酚妥拉明和胍乙啶处理过的兔薄肌进行活体显微镜检查，研究神经诱导的血管舒张。对薄肌神经进行神经刺激可诱导血管舒张，这种舒张与频率和脉冲持续时间相关，对阿托品和普萘洛尔不敏感，但可被河豚毒素消除。一氧化氮合酶抑制剂Nω-硝基-L-精氨酸甲酯（L-NAME，100微摩尔），而非其对映体D-NAME，显著抑制神经刺激或外源性P物质或神经激肽A诱导的血管舒张。降钙素基因相关肽、前列腺素E2或硝普钠引起的血管舒张不受影响。P物质拮抗剂spantide（30微摩尔）与L-NAME一样，显著减弱神经诱导的血管舒张。我们的结果表明，骨骼肌中神经诱导的血管舒张可归因于P物质和/或其他速激肽的释放，并且一氧化氮随后介导对神经释放的内源性速激肽的反应。
