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- D M Roden
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
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- P B Bennett
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
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- D J Snyders
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
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- J R Balser
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
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- L M Hondeghem
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
説明
<jats:p>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.</jats:p>
収録刊行物
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- Circulation Research
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Circulation Research 62 (5), 1055-1058, 1988-05
Ovid Technologies (Wolters Kluwer Health)
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詳細情報 詳細情報について
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- CRID
- 1363670320313228288
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- ISSN
- 15244571
- 00097330
- http://id.crossref.org/issn/00097330
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- データソース種別
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- Crossref