Kamata K, Umeda F, Kasuya Y
Department of Physiology and Morphology, Hoshi University, Tokyo, Japan.
J Cardiovasc Pharmacol. 1996 Apr;27(4):601-6. doi: 10.1097/00005344-199604000-00022.
Both acetylcholine (ACh) and cyclopiazonic acid (CPA) caused vasodilation of the mesenteric arterial bed in a concentration-dependent manner. When the mesenteric arterial bed was perfused with 0.1% Triton X-100 for 30 s, ACh- or CPA-induced vasodilation was almost abolished. ACh-induced vasodilation was significantly attenuated in isotonic high K+ (60 mM) solution and significantly decreased by treatment with methylene blue (MB) with NG-nitro-L-arginine (L-NNA) in isotonic high K+ (60 mM) solution, whereas CPA-induced vasodilation of the mesentery was not affected by these treatments. ACh- or CPA-induced vasodilation was not affected by indomethacin. ACh caused significant increase in cyclic GMP levels and cyclic AMP in effluents from the perfused mesentery, whereas CPA could not increase cyclic GMP. CPA caused significant increase in cyclic AMP in a concentration-dependent manner, and CPA-induced increase in cyclic AMP was completely inhibited by removal of the endothelium. These results suggest that one or more endothelium-derived relaxing factor (EDRF) or factors should exist other than endothelium-derived nitric oxide (EDNO) or endothelium-derived hyperpolarizing factor (EDHF) in the endothelium of the rat mesenteric arterial bed. The novel EDRF may relax the mesenteric arterial bed through production of cyclic AMP but not cyclic GMP.
乙酰胆碱（ACh）和环匹阿尼酸（CPA）均以浓度依赖性方式引起肠系膜动脉床血管舒张。当用0.1% Triton X-100灌注肠系膜动脉床30秒时，ACh或CPA诱导的血管舒张几乎被消除。在等渗高钾（60 mM）溶液中，ACh诱导的血管舒张明显减弱，并且在等渗高钾（60 mM）溶液中用亚甲蓝（MB）与NG-硝基-L-精氨酸（L-NNA）处理后显著降低，而CPA诱导的肠系膜血管舒张不受这些处理的影响。ACh或CPA诱导的血管舒张不受吲哚美辛影响。ACh导致灌注肠系膜流出液中环状鸟苷酸（cGMP）水平和环状腺苷酸（cAMP）显著升高，而CPA不能增加cGMP。CPA以浓度依赖性方式导致cAMP显著升高，并且去除内皮后，CPA诱导的cAMP升高被完全抑制。这些结果表明，大鼠肠系膜动脉床内皮中除了内皮源性一氧化氮（EDNO）或内皮源性超极化因子（EDHF）之外，应该存在一种或多种内皮源性舒张因子（EDRF）。这种新型的EDRF可能通过产生cAMP而不是cGMP来舒张肠系膜动脉床。
