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Downregulation of voltage-gated K(+) channels in rat heart with right ventricular hypertrophy

J K Lee1, A Nishiyama, F Kambe

  • 1Department of Circulation, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan 464-8601, USA.

The American Journal of Physiology
|November 24, 1999
PubMed

Insights

Myocardial hypertrophy in rats significantly alters voltage-gated potassium channel mRNA expression, impacting ventricular repolarization. This study investigates the link between hypertrophy and changes in Kv channel gene expression.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Pharmacology

Background:

  • Myocardial hypertrophy is a significant risk factor for cardiac dysfunction.
  • Voltage-gated potassium (Kv) channels play a crucial role in cardiac repolarization.
  • Pulmonary hypertension can lead to myocardial hypertrophy and altered cardiac electrophysiology.

Purpose of the Study:

  • To investigate the impact of monocrotaline (MCT)-induced pulmonary hypertension on myocardial hypertrophy.
  • To examine the changes in mRNA expression levels of various voltage-gated potassium (Kv) channels in hypertrophied rat ventricles.
  • To correlate alterations in Kv channel gene expression with changes in ventricular repolarization.

Main Methods:

  • Induction of pulmonary hypertension and myocardial hypertrophy in rats using monocrotaline (MCT).
  • Assessment of cardiac hypertrophy via right ventricle weight to left ventricle plus septum weight ratio.
  • Electrocardiographic recordings to measure QRS duration, Q-T interval, and corrected Q-T interval (Q-T(c)).
  • Quantification of mRNA levels for multiple Kv channel subtypes (Kv1.2, 1.4, 1.5, 2.1, 4.2, 4.3) using ribonuclease protection assays at different time points (day 14 and day 28).

Main Results:

  • MCT-induced rats showed significant myocardial hypertrophy by day 28.
  • Prolonged QRS duration, Q-T interval, and Q-T(c) were observed in MCT rats on day 28.
  • Significant downregulation of mRNA levels for Kv1.2, Kv1.5, Kv2.1, Kv4.2, and Kv4.3 was found by day 28, while Kv1.4 remained unaffected.
  • No significant changes in Kv channel mRNA levels were observed at the earlier time point (day 14).

Conclusions:

  • Advanced-stage myocardial hypertrophy in MCT-induced pulmonary hypertension is associated with significant alterations in ventricular repolarization.
  • The observed changes in repolarization are likely due to the inhibition of gene expression of multiple voltage-gated potassium channel subtypes.
  • These findings highlight a potential molecular mechanism linking hypertrophy to electrical remodeling and cardiac dysfunction.

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