Academic Journal

Quinidine delays IK activation in guinea pig ventricular myocytes.

التفاصيل البيبلوغرافية
العنوان: Quinidine delays IK activation in guinea pig ventricular myocytes.
المؤلفون: Roden, D M, Bennett, P B, Snyders, D J, Balser, J R, Hondeghem, L M
المصدر: Circulation Research ; volume 62, issue 5, page 1055-1058 ; ISSN 0009-7330 1524-4571
بيانات النشر: Ovid Technologies (Wolters Kluwer Health)
سنة النشر: 1988
الوصف: A major action of the antiarrhythmic agent quinidine is prolongation of cardiac repolarization. In these experiments, the time-dependent effects of quinidine on the delayed rectifier potassium current, IK, a current contributing to cardiac repolarization, were investigated in acutely disaggregated guinea pig ventricular myocytes using the whole-cell recording configuration of the patch-clamp method. The effect of quinidine on IK was dependent on the duration of depolarization. After long (2,000 msec) pulses, IK was reduced by 30 +/- 27% (SD; n = 8, paired) by 10 microM quinidine; in contrast, after short (100 msec) pulses, the drug decreased IK 65 +/- 35% (p less than 0.05). This effect was found both in paired experiments as well as when quinidine-pretreated cells were compared to non-pretreated cells. Quinidine significantly delayed IK activation (9 +/- 20 msec at baseline vs. 44 +/- 25 msec in drug, p less than 0.05), but did not alter the subsequent time course of activation (time constant 659 +/- 118 msec). These findings are consistent with the hypothesis that quinidine promotes occupancy of a channel state from which opening does not occur.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1161/01.res.62.5.1055
DOI: 10.1161/01.RES.62.5.1055
الاتاحة: http://dx.doi.org/10.1161/01.res.62.5.1055
https://www.ahajournals.org/doi/pdf/10.1161/01.RES.62.5.1055
رقم الانضمام: edsbas.B1689A08
قاعدة البيانات: BASE
الوصف
DOI:10.1161/01.res.62.5.1055