Kamata K, Hosokawa M
Department of Physiology and Morphology, Hoshi University, Tokyo, Japan.
Res Commun Mol Pathol Pharmacol. 1997 Apr;96(1):57-70.
The vasodilator effects of acetylcholine were examined in methoxamine-preconstricted perfused kidneys taken from rats with streptozotocin (STZ)-induced diabetes. Acetylcholine-dependent vasodilatation was significantly weaker in STZ-induced diabetic rats than in age-matched controls, and it was completely abolished by treatment with 60 mM K+ plus NG-nitro-L-arginine (L-NNA) plus methylene blue in the control rats and was significantly but not completely inhibited by these treatment in the diabetic rats. Although acetylcholine-induced vasodilation was not affected by indomethacin in control rats, it was attenuated by indomethacin in the diabetic rats. Arachidonic acid-induced vasoconstriction was slightly but significantly increased in the diabetic rats. Acetylcholine increased significantly the level of 6-keto-prostaglandin F1 alpha in the effluent from perfused kidneys from diabetic rats. These results suggest that the endothelium-dependent vasodilatation induced by acetylcholine in the renal vascular bed of age-matched control rats is due to the release of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), whereas the vasodilatation induced by acetylcholine in the STZ-diabetic kidney also involves prostaglandin I2 as well as NO and EDHF.
在取自链脲佐菌素（STZ）诱导的糖尿病大鼠的甲氧明预收缩灌注肾中检测了乙酰胆碱的血管舒张作用。与年龄匹配的对照大鼠相比，STZ诱导的糖尿病大鼠中乙酰胆碱依赖性血管舒张明显较弱，在对照大鼠中用60 mM K⁺加NG-硝基-L-精氨酸（L-NNA）加亚甲蓝处理可完全消除这种血管舒张，而在糖尿病大鼠中这些处理可显著但不完全抑制血管舒张。虽然在对照大鼠中乙酰胆碱诱导的血管舒张不受吲哚美辛影响，但在糖尿病大鼠中吲哚美辛可使其减弱。花生四烯酸诱导的血管收缩在糖尿病大鼠中略有但显著增加。乙酰胆碱显著增加了糖尿病大鼠灌注肾流出液中6-酮-前列腺素F1α的水平。这些结果表明，在年龄匹配的对照大鼠肾血管床中，乙酰胆碱诱导的内皮依赖性血管舒张是由于一氧化氮（NO）和内皮衍生的超极化因子（EDHF）的释放，而在STZ糖尿病肾中，乙酰胆碱诱导的血管舒张还涉及前列腺素I2以及NO和EDHF。
