RENA EATED DOGS

乙酰胆碱引起肾血管收缩的机制 (ACh)在接受吲哚美辛（Indo）治疗的犬中， 输注维拉帕米（V）或二丁酰环腺苷酸（db-AMP）。 肾 动脉输注V（60 μ g/min）可减弱，但不能消除， Indo处理犬ACh（40 μ g/min）诱导的肾血浆流量下降 （5 mg/kg）。 而肾素分泌率则无升高趋势。 肾 动脉灌注db-cAMP（6 mg/min）恢复了利钠尿肽， ACh在Indo处理的狗中的血管舒张作用。 数据表明 ACh通过刺激细胞内CA ++浓度增加， 细胞内Ca~（++）内流和胞内贮存部位Ca~（++）释放 印度治疗狗。 细胞质Ca ++浓度的增加导致 血管平滑肌收缩导致肾脏 血管收缩

The mechanism for the renal vasoconstriction induced by acetylocholine (ACh) in idomethacin (Indo)-treated dogs was examined in dogs receiving an infusion of either verapamil (V) or dibutyryl cyclic AMP (db-AMP). Renal arterial infusion of V (60 ug/min) attenuated, but did not eliminate, the fall in renal plasma flow induced by ACh (40 ug/min) in Indo-treated dogs (5 mg/kg). Renin secretory rate, however, did not show a rise. Renal arterial infusion of db-cAMP (6 mg/min) restored the natriuretic and vasodilatory effects of ACh in Indo-treated dogs. The data suggest 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.