Burgaud J L, Oudart N
Laboratoire de Pharmacologie, UFR de Pharmacie, Limoges, France.
J Pharm Pharmacol. 1994 Feb;46(2):153-5. doi: 10.1111/j.2042-7158.1994.tb03762.x.
A role for nitric oxide in the H3-histaminergic agonist-induced inhibition of the non-adrenergic, non-cholinergic (NANC) contraction has been studied in guinea-pig perfused bronchioles. (R)-alpha-Methylhistamine ((R)-alpha-MeHA), an agonist for H3 receptors, inhibited the NANC contraction induced by electrical field stimulation. NG-Nitro-L-arginine methyl ester (L-NAME) (50 microM), an inhibitor of nitric oxide synthesis, blocked the effect of (R)-alpha-MeHA. The effect of L-NAME was reversed by L-arginine (50 microM). L-NAME, L-arginine or (R)-alpha-MeHA were without effect on exogenous substance P- or neurokinin A-induced contractile responses of the perfused bronchioles. These results show that an H3-agonist inhibited the release of neurotransmitters in NANC nerve endings of guinea-pig perfused bronchioles presumably by production of nitric oxide.
在豚鼠灌注细支气管中,已对一氧化氮在H3组胺能激动剂诱导的非肾上腺素能、非胆碱能(NANC)收缩抑制中的作用进行了研究。H3受体激动剂(R)-α-甲基组胺((R)-α-MeHA)抑制电场刺激诱导的NANC收缩。一氧化氮合成抑制剂NG-硝基-L-精氨酸甲酯(L-NAME)(50微摩尔)阻断了(R)-α-MeHA的作用。L-精氨酸(50微摩尔)可逆转L-NAME的作用。L-NAME、L-精氨酸或(R)-α-MeHA对外源性P物质或神经激肽A诱导的灌注细支气管收缩反应均无影响。这些结果表明,H3激动剂可能通过产生一氧化氮来抑制豚鼠灌注细支气管NANC神经末梢中神经递质的释放。