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Modulation of cardiac L-type Ca2+ current by angiotensin-(1-7): normal versus heart failure

Peng Zhou1, Che Ping Cheng1, Tiankai Li2

  • 1Section on Cardiovascular Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.

Therapeutic Advances in Cardiovascular Disease
|June 18, 2015
PubMed

Insights

In heart failure (HF), angiotensin-(1-7) [Ang-(1-7)] increases L-type calcium current (ICa,L) in myocytes. This effect, mediated by Mas receptors, involves nitric oxide and bradykinin pathways, offering potential therapeutic insights.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Electrophysiology

Background:

  • Angiotensin-(1-7) [Ang-(1-7)] counteracts angiotensin II effects in heart failure (HF).
  • Ang-(1-7) exhibits positive inotropic effects on the left ventricle (LV) and myocytes.
  • The electrophysiological mechanisms of Ang-(1-7) in HF remain unclear.

Purpose of the Study:

  • Investigate the role of Ang-(1-7) in modulating LV myocyte L-type calcium current (ICa,L).
  • Elucidate the underlying electrophysiological mechanisms of Ang-(1-7) in normal and HF states.

Main Methods:

  • Utilized the patch clamp technique on isolated LV myocytes from rats with isoproterenol-induced HF and age-matched controls.
  • Compared the effects of Ang-(1-7) (10⁻⁵ M) on ICa,L in normal and HF myocytes.
  • Assessed the involvement of nitric oxide (NO) and bradykinin (BK) pathways using specific inhibitors (L-NAME, HOE 140) and the Mas receptor antagonist (A-779).

Main Results:

  • Ang-(1-7) had no significant effect on ICa,L in normal myocytes.
  • In HF myocytes, baseline ICa,L was reduced, and Ang-(1-7) significantly increased ICa,L by 21%.
  • The Ang-(1-7) induced increase in ICa,L was potentiated by NO synthase inhibition and attenuated by BK inhibition, and abolished by Mas receptor blockade.

Conclusions:

  • Heart failure alters the electrophysiological response of ICa,L to Ang-(1-7).
  • Ang-(1-7) enhances ICa,L in HF myocytes, contrasting with its lack of effect in normal myocytes.
  • These beneficial effects are mediated via Ang-(1-7) Mas receptors and involve the activation of NO/BK signaling pathways.
Abstract

Keywords:
calciumheart failureion currentsreceptorsvasodilator agents

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