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Published on: May 5, 2020

Amlodipine ameliorates myocardial hypertrophy by inhibiting EGFR phosphorylation

Yulin Liao1, Masanori Asakura, Seiji Takashima

  • 1Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0781, Japan.

Biochemical and Biophysical Research Communications
|January 18, 2005
PubMed

Insights

Amlodipine, a calcium channel blocker, reduces cardiac hypertrophy by inhibiting epidermal growth factor receptor (EGFR) phosphorylation. This study shows amlodipine

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Pharmacology

Background:

  • Pressure overload-induced cardiac hypertrophy mechanisms are not fully understood.
  • Epidermal growth factor receptor (EGFR) phosphorylation is implicated in cardiomyocyte hypertrophy.
  • Long-acting calcium channel blockers' effects on cardiac hypertrophy require further investigation.

Purpose of the Study:

  • To investigate amlodipine's effect on pressure overload-induced cardiac hypertrophy.
  • To determine if amlodipine attenuates cardiac hypertrophy by inhibiting EGFR phosphorylation.

Main Methods:

  • In vitro: Amlodipine's effect on epinephrine-induced protein synthesis and EGFR phosphorylation in neonatal rat cardiomyocytes.
  • In vivo: Amlodipine's effect on transverse aortic constriction (TAC)-induced cardiac hypertrophy in C57/B6 mice.

Main Results:

  • Amlodipine dose-dependently inhibited protein synthesis and EGFR phosphorylation in cultured cardiomyocytes.
  • Amlodipine treatment significantly reduced the heart-to-body weight ratio in TAC mice.
  • Amlodipine ameliorated myocardial hypertrophy in vivo.

Conclusions:

  • Amlodipine attenuates cardiac hypertrophy by inhibiting EGFR phosphorylation.
  • Amlodipine demonstrates therapeutic potential for pressure overload-induced cardiac hypertrophy.

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