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异丙肾上腺素使心脏钾电流失活的新作用不受β和α肾上腺素能阻滞剂的阻断。

A novel action of isoproterenol to inactivate a cardiac K+ current is not blocked by beta and alpha adrenergic blockers.

作者信息

Tromba C, Cohen I S

机构信息

Department of Physiology and Biophysics, State University of New York, Stony Brook 11794.

出版信息

Biophys J. 1990 Sep;58(3):791-5. doi: 10.1016/S0006-3495(90)82422-X.

Abstract

The K+ current iKl sets the resting potential in cardiac cells. Here we report that isoproterenol (ISO), a prototypical beta agonist, increases inactivation of iKl. This action of ISO on iKl is mimicked by permeant analogues of cAMP but is not blocked by the beta blockers propranolol and pindolol or the alpha blockers prazosin or yohimbine. We suggest that this novel action of ISO may contribute to pacemaker activity in the Purkinje strand and be mediated through a class of receptors different from classical beta's or alpha's.

摘要

钾离子电流iKl决定了心脏细胞的静息电位。在此我们报告,典型的β激动剂异丙肾上腺素(ISO)可增加iKl的失活。ISO对iKl的这种作用可被cAMP的渗透性类似物模拟,但不受β阻滞剂普萘洛尔和吲哚洛尔或α阻滞剂哌唑嗪或育亨宾的阻断。我们认为,ISO的这种新作用可能有助于浦肯野纤维束中的起搏活动,并通过一类不同于经典β或α受体的受体介导。

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