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Non-neuronal cholinergic machinery present in cardiomyocytes offsets hypertrophic signals

Cibele Rocha-Resende1, Ashbeel Roy, Rodrigo Resende

  • 1Department of Physiology and Biophysics, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG, CEP 31270-901, Brazil. cibeler@ufmg.br

Journal of Molecular and Cellular Cardiology
|May 17, 2012
PubMed

Insights

Cardiomyocytes produce acetylcholine (ACh), a key molecule for heart health. This study reveals that cardiac ACh signaling protects the heart against hypertrophy and malfunction, enhancing parasympathetic nervous system effects.

Area of Science:

  • Cardiovascular Physiology
  • Neuroendocrinology
  • Molecular Cardiology

Background:

  • Acetylcholine (ACh) plays a vital role in cardiac function, with reduced levels linked to heart failure.
  • Cardiomyocytes possess the machinery to secrete ACh, suggesting a potential intrinsic protective mechanism.
  • The functionality of this non-neuronal cholinergic system in cardiomyocytes requires further investigation.

Purpose of the Study:

  • To investigate the functional significance of cardiomyocyte-derived ACh in cardiac protection.
  • To determine if enhancing ACh availability in cardiomyocytes can counteract detrimental effects of adrenergic stimulation.
  • To explore the interplay between cholinergic and adrenergic signaling in the heart.

Main Methods:

  • Utilized cholinesterase inhibitors and siRNA targeting acetylcholinesterase (AChE) to increase ACh availability in cardiomyocytes.
  • Measured nitric oxide (NO) formation as a biosensor for ACh release.
  • Assessed hypertrophic responses, molecular changes, and calcium handling in cardiomyocytes under adrenergic stimulation.

Main Results:

  • Cholinesterase inhibition significantly increased NO levels in ventricular myocytes, indicating functional ACh release.
  • This effect was blocked by atropine (muscarinic antagonist) and inhibition of ACh synthesis or storage.
  • Cholinesterase inhibition attenuated adrenergic-induced cardiomyocyte hypertrophy, molecular alterations, and calcium transient dysfunction.
  • Inhibition of ACh storage or muscarinic receptor blockade blunted the anti-hypertrophic effects of cholinesterase inhibition.
  • Adrenergic stimulation was found to upregulate components of the cardiac cholinergic system.

Conclusions:

  • Cardiomyocytes possess a functional cholinergic system that provides protection against hyperadrenergic stimulation.
  • This intrinsic cholinergic signaling may amplify parasympathetic protective effects and counteract cardiac hypertrophy.
  • The findings highlight a novel mechanism for cardiac self-regulation and protection.

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