Changes in the mRNA levels of delayed rectifier potassium channels in human atrial fibrillation

Ling Ping Lai, Ming Jai Su, Jiunn Lee Lin, Fang Yue Lin, Chang Her Tsai, Yih Sharng Chen, Yung Zu Tseng, Wen Pin Lien, Shoei K. Stephen Huang

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Introduction: We measured mRNA levels of delayed rectifier potassium channels in human atrial tissue to investigate the mechanism of the shortening of the atrial effective refractory period and the loss of rate-adaptive shortening of the atrial effective refractory period in human atrial fibrillation. Methods and Results: A total of 34 patients undergoing open heart surgery were included. Atrial tissue was obtained from the right atrial free wall, right atrial appendage, left atrial free wall and left atrial appendage, respectively. The mRNA amounts of K(VLQT1) (I(Ks)), minK (β-subunit of I(Ks)), HERG (I(Kr)), and K(V1.5) (I(Kur)) were measured by reverse transcription-polymerase chain reaction and normalized to the mRNA amount of GAPDH. We found that the mRNA levels of K(V1.5), HERG and K(VLQT1) were all significantly decreased in patients with persistent atrial fibrillation for more than 3 months. In contrast, the mRNA level of minK was significantly increased in patients with persistent atrial fibrillation for more than 3 months. We further showed that these changes were independent of the underlying cardiac disease, atrial filling pressure, gender and age. We also found that there was no spatial dispersion of mRNA levels among the four atrial sampling sites. Conclusions: Because the decrease in potassium currents results in a prolonged action potential, the shortening of the atrial effective refractory period in atrial fibrillation should be attributed to other factors. However, the decrease in I(Ks) might contribute, at least in part, to the loss of rate-adaptive shortening of the atrial refractory period. Copyright (C) 2000 S. Karger AG, Basel.

Original languageEnglish
Pages (from-to)248-255
Number of pages8
JournalCardiology
Volume92
Issue number4
DOIs
Publication statusPublished - Jan 1 1999
Externally publishedYes

Fingerprint

Delayed Rectifier Potassium Channels
Atrial Fibrillation
Messenger RNA
Mink
Atrial Appendage
Atrial Pressure
Thoracic Surgery
Action Potentials
Reverse Transcription
Heart Diseases
Potassium
Polymerase Chain Reaction

Keywords

  • Atrial fibrillation
  • Delayed rectifier potassium channels
  • Potassium channels

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology (medical)

Cite this

Lai, L. P., Su, M. J., Lin, J. L., Lin, F. Y., Tsai, C. H., Chen, Y. S., ... Stephen Huang, S. K. (1999). Changes in the mRNA levels of delayed rectifier potassium channels in human atrial fibrillation. Cardiology, 92(4), 248-255. https://doi.org/10.1159/000006982

Changes in the mRNA levels of delayed rectifier potassium channels in human atrial fibrillation. / Lai, Ling Ping; Su, Ming Jai; Lin, Jiunn Lee; Lin, Fang Yue; Tsai, Chang Her; Chen, Yih Sharng; Tseng, Yung Zu; Lien, Wen Pin; Stephen Huang, Shoei K.

In: Cardiology, Vol. 92, No. 4, 01.01.1999, p. 248-255.

Research output: Contribution to journalArticle

Lai, LP, Su, MJ, Lin, JL, Lin, FY, Tsai, CH, Chen, YS, Tseng, YZ, Lien, WP & Stephen Huang, SK 1999, 'Changes in the mRNA levels of delayed rectifier potassium channels in human atrial fibrillation', Cardiology, vol. 92, no. 4, pp. 248-255. https://doi.org/10.1159/000006982
Lai, Ling Ping ; Su, Ming Jai ; Lin, Jiunn Lee ; Lin, Fang Yue ; Tsai, Chang Her ; Chen, Yih Sharng ; Tseng, Yung Zu ; Lien, Wen Pin ; Stephen Huang, Shoei K. / Changes in the mRNA levels of delayed rectifier potassium channels in human atrial fibrillation. In: Cardiology. 1999 ; Vol. 92, No. 4. pp. 248-255.
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AU - Tsai, Chang Her

AU - Chen, Yih Sharng

AU - Tseng, Yung Zu

AU - Lien, Wen Pin

AU - Stephen Huang, Shoei K.

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N2 - Introduction: We measured mRNA levels of delayed rectifier potassium channels in human atrial tissue to investigate the mechanism of the shortening of the atrial effective refractory period and the loss of rate-adaptive shortening of the atrial effective refractory period in human atrial fibrillation. Methods and Results: A total of 34 patients undergoing open heart surgery were included. Atrial tissue was obtained from the right atrial free wall, right atrial appendage, left atrial free wall and left atrial appendage, respectively. The mRNA amounts of K(VLQT1) (I(Ks)), minK (β-subunit of I(Ks)), HERG (I(Kr)), and K(V1.5) (I(Kur)) were measured by reverse transcription-polymerase chain reaction and normalized to the mRNA amount of GAPDH. We found that the mRNA levels of K(V1.5), HERG and K(VLQT1) were all significantly decreased in patients with persistent atrial fibrillation for more than 3 months. In contrast, the mRNA level of minK was significantly increased in patients with persistent atrial fibrillation for more than 3 months. We further showed that these changes were independent of the underlying cardiac disease, atrial filling pressure, gender and age. We also found that there was no spatial dispersion of mRNA levels among the four atrial sampling sites. Conclusions: Because the decrease in potassium currents results in a prolonged action potential, the shortening of the atrial effective refractory period in atrial fibrillation should be attributed to other factors. However, the decrease in I(Ks) might contribute, at least in part, to the loss of rate-adaptive shortening of the atrial refractory period. Copyright (C) 2000 S. Karger AG, Basel.

AB - Introduction: We measured mRNA levels of delayed rectifier potassium channels in human atrial tissue to investigate the mechanism of the shortening of the atrial effective refractory period and the loss of rate-adaptive shortening of the atrial effective refractory period in human atrial fibrillation. Methods and Results: A total of 34 patients undergoing open heart surgery were included. Atrial tissue was obtained from the right atrial free wall, right atrial appendage, left atrial free wall and left atrial appendage, respectively. The mRNA amounts of K(VLQT1) (I(Ks)), minK (β-subunit of I(Ks)), HERG (I(Kr)), and K(V1.5) (I(Kur)) were measured by reverse transcription-polymerase chain reaction and normalized to the mRNA amount of GAPDH. We found that the mRNA levels of K(V1.5), HERG and K(VLQT1) were all significantly decreased in patients with persistent atrial fibrillation for more than 3 months. In contrast, the mRNA level of minK was significantly increased in patients with persistent atrial fibrillation for more than 3 months. We further showed that these changes were independent of the underlying cardiac disease, atrial filling pressure, gender and age. We also found that there was no spatial dispersion of mRNA levels among the four atrial sampling sites. Conclusions: Because the decrease in potassium currents results in a prolonged action potential, the shortening of the atrial effective refractory period in atrial fibrillation should be attributed to other factors. However, the decrease in I(Ks) might contribute, at least in part, to the loss of rate-adaptive shortening of the atrial refractory period. Copyright (C) 2000 S. Karger AG, Basel.

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