RENAL VASOCONSTRICTION INDUCED BY ACETYLCHOLINE IN INDOMETHACIN-TREATED DOGS

黄曲霉毒素引起肾血管收缩的机制研究 用消炎痛(INDO)处理犬的乙酰胆碱(ACh) 接受去甲二氢愈创木素输注的犬的检查 脂氧合酶抑制剂酸(NDGA)或钙剂地尔硫卓(D) 进入拦截器。肾动脉注射NDGA(6 mg/min) 不能阻止ACh对肾血管的收缩作用。肾动脉 D(60毫克/分钟)的输注有所减弱，但并未消除 总的来说，肾脏血浆流量和钠排泄的下降 用ACh(40µg/min)诱发5 mg/kg吲哚青霉素狗模型。 然而，肾素分泌率并没有上升。数据 提示ACh对INDO治疗后肾血管的收缩作用 狗并不是脂氧合酶活性增加的结果。 这些数据进一步表明，ACh会导致 细胞内钙离子浓度通过刺激钙离子内流和 印支流中细胞内储存部位钙离子的释放 治疗过的狗。胞浆内钙离子浓度的升高 导致血管平滑肌收缩，导致肾脏 血管收缩。

The mechanism for the renal vasoconstriction induced by acetylcholine (ACh) in indomethacin (Indo)-treated dogs was examined in dogs receiving an infusion of nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, or diltiazem (D), a calcium entry blocker. Renal arterial infusion of NDGA (6 mg/min) did not prevent the renal vasoconstriction by ACh. Renal arterial infusion of D (60 Mug/min) attenuated, but did not eliminate entirely, the fall in renal plasma flow and sodium excretion induced by ACh (40 Mug/min) in Indo-treated dogs (5 mg/kg). Renin secretory rate, however, did not show a rise. The data suggest that the renal vasoconstriction by ACh in Indo-treated dogs does not result from an increase in lipoxygenase activity. The data suggest further that ACh causes an increase in intracellular Ca++ concentration by stimulating Ca++ influx and the release of Ca++ from intracellular storage sites in Indo- treated dogs. The increase in cytosolic Ca++ concentration then leads to contraction of vascular smooth muscle resulting in renal vasoconstriction.