Abstract：
:It has been reported that naloxone, an opioid antagonist, has antiarrhythmic activity in vivo. In Langendorff perfused rat hearts, we found that ischemia-reperfusion-induced ventricular tachyarrhythmia reverted to normal sinus rhythm after the treatment with naloxone (3 approximately 10 microM). The method of voltage and current clamp were used to study the underlying mechanism of its antiarrhythmic activity on isolated cardiac myocytes. In isolated rat ventricular and in guinea-pig and human atrial myocytes, naloxone prolonged the action potential duration reversibly. In rat ventricular myocytes, naloxone (1 approximately 30 microM) inhibited sodium current (I(Na)), transient outward potassium current (I(to)), and calcium current (I(Ca)). On the contrary, the addition of naloxone significantly increased inward rectifier potassium current (I(K1)). For the effect on I(Na), naloxone did not shift the inactivation curve of I(Na) but retarded the I(Na) recovery rate from inactivation state. Naloxone suppressed I(to) with a significant left-shift of the inactivation curve, however, the time course of I(to) recovery from inactivation was not affected. In guinea pig atrial myocytes, naloxone (10 microM) decreased the delayed rectifier K+ current (IK). These results show that naloxone exert various extent of inhibition on I(Na), I(to), IK and I(Ca). The prolongation of cardiac action potential is related to the inhibition of I(to) and IK. The antiarrhythmic activity of naloxone is more closely related to the inhibition of Na+ and K+ currents rather than the blockade of myocardial opioid receptors.
journal_name
Life Scijournal_title
Life sciencesauthors
Hung CF,Wu MH,Tsai CH,Chu SH,Chi JF,Su MJdoi
10.1016/s0024-3205(98)00383-xsubject
Has Abstractpub_date
1998-01-01 00:00:00pages
1205-19issue
14eissn
0024-3205issn
1879-0631pii
S002432059800383Xjournal_volume
63pub_type
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