RENAL VASOCONSTRICTION INDUCED BY ACETYLCHOLINE IN INDOMETHACIN-TREATED DOGS

乙酰胆碱在吲哚美辛治疗的狗中引起的肾血管收缩

• 批准号: 3942834
• 负责人: J YUN
• 金额: --
• 依托单位: NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3942834
• 关键词: acetylcholine; cardiovascular pharmacology; hypertension; indomethacin; kidney circulation; kidney pharmacology; muscle contraction; renin; saluresis; vascular smooth muscle; vasoconstriction

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.

致肾血管收缩的机制 吲哚美辛（Indo）治疗犬的乙酰胆碱（ACh） 在接受去甲二氢愈创木酸输注的犬中检查 脂肪氧合酶抑制剂，或地尔硫卓（D），钙 进入拦截器。 肾动脉灌注NDGA（6 mg/min） 不能阻止ACh引起的肾血管收缩。 肾动脉 输注D（60 μ g/min）可减弱，但不能消除 肾血浆流量和钠排泄的下降 在Indo处理的狗（5 mg/kg）中由ACh（40 μ g/min）诱导。 而肾素分泌率则无升高趋势。 数据 表明ACh引起的肾血管收缩在吲哚美辛治疗的 狗的死亡不是由于脂氧合酶活性的增加。 数据进一步表明，ACh导致 细胞内Ca++浓度通过刺激Ca++内流和 细胞内储存点Ca ~（++）的释放 治疗狗 细胞内Ca++浓度的增加， 导致血管平滑肌收缩， 血管收缩