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钠钾-ATP酶在合成心房利钠因子血管舒张作用中的作用。

The role of Na+-K+ -ATPase in the vasorelaxant actions of synthetic atrial natriuretic factor.

作者信息

Sybertz E J, Desiderio D M

出版信息

Arch Int Pharmacodyn Ther. 1985 Nov;278(1):142-9.

PMID:2420296
Abstract

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.

摘要

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。

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