Sybertz E J, Desiderio D M
Arch Int Pharmacodyn Ther. 1985 Nov;278(1):142-9.
The present study evaluated the role of Na+-K+ -ATPase stimulation in the relaxant response to synthetic atrial natriuretic factor (atriopeptin II; ANF) in norepinephrine (0.18 microM)-contracted rabbit aorta. ANF (10(-10)-10(-7) M) produced a concentration-related relaxation of NE-contracted aortic rings. The calculated concentration required to produce 50 per cent relaxation (EC50) was 5 +/- 3 X 10(-9) M. ANF-induced relaxation was significantly attenuated by ouabain (30 microM). Likewise, ANF (10(-7) and 5 X 10(-9) M) elicited significantly less relaxation of aortic rings contracted with norepinephrine in a physiological salt solution containing zero KCl. Nitroprusside-induced relaxation also was attenuated by ouabain and in zero KCl salt solution. The data suggest that synthetic ANF induces relaxation in rabbit aortic rings by a ouabain and KCl sensitive mechanism, presumably Na+-K+ -ATPase.
本研究评估了在去甲肾上腺素（0.18微摩尔）收缩的兔主动脉中，钠钾ATP酶刺激在对合成心房利钠因子（心钠素II；ANF）舒张反应中的作用。ANF（10^-10 - 10^-7 M）使NE收缩的主动脉环产生浓度依赖性舒张。产生50%舒张所需的计算浓度（EC50）为5±3×10^-9 M。哇巴因（30微摩尔）显著减弱了ANF诱导的舒张。同样，在含零氯化钾的生理盐溶液中，ANF（10^-7和5×10^-9 M）引起的去甲肾上腺素收缩的主动脉环舒张明显减少。硝普钠诱导的舒张也被哇巴因减弱，且在零氯化钾盐溶液中也是如此。数据表明，合成ANF通过一种对哇巴因和氯化钾敏感的机制，可能是钠钾ATP酶，诱导兔主动脉环舒张。
