Whittle B J, Lopez-Belmonte J, Moncada S
Department of Pharmacology, Wellcome Research Laboratories, Beckenham, Kent, UK.
Eur J Pharmacol. 1992 Aug 6;218(2-3):339-41. doi: 10.1016/0014-2999(92)90188-a.
The role of endogenous nitric oxide (NO) in the gastric mucosal vasodilatation induced by acute intragastric perfusion with capsaicin or close-arterial infusion of rat alpha-calcitonin gene-related peptide (CGRP) was evaluated in the pentobarbitone-anaesthetised rat using laser Doppler flowmetry (LDF). The mucosal vasodilatation induced by intraluminal capsaicin (160 microM) was dose dependently reduced by the inhibitor of NO synthesis, NG-nitro-L-arginine methyl ester (L-NAME; 1-5 mg kg-1 i.v.), effects reversed by concurrent administration of L-arginine (100 mg kg-1 i.v.). L-NAME (2 mg kg-1) induced a small reduction in the mucosal vasodilatation induced by close-arterial infusion of rat alpha-CGRP (50 pmol kg-1 min-1). These findings indicate a role of NO in the gastric vasodilatation induced by stimulation of sensory neurones with intragastric capsaicin.
在戊巴比妥麻醉的大鼠中，使用激光多普勒血流仪（LDF）评估内源性一氧化氮（NO）在辣椒素急性胃内灌注或大鼠α-降钙素基因相关肽（CGRP）动脉内灌注诱导的胃黏膜血管舒张中的作用。一氧化氮合成抑制剂NG-硝基-L-精氨酸甲酯（L-NAME；1-5mg kg-1静脉注射）可剂量依赖性地降低腔内辣椒素（160μM）诱导的黏膜血管舒张，同时给予L-精氨酸（100mg kg-1静脉注射）可逆转这种作用。L-NAME（2mg kg-1）可使大鼠α-CGRP动脉内灌注（50pmol kg-1 min-1）诱导的黏膜血管舒张略有降低。这些发现表明NO在胃内辣椒素刺激感觉神经元诱导的胃血管舒张中起作用。
