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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

G protein-mediated inhibitory effect of a nitric oxide donor on the L-type Ca2+ current in rat ventricular myocytes

N Abi-Gerges1, R Fischmeister, P F Méry

  • 1Laboratoire de Cardiologie Cellulaire & Moleculaire, INSERM U-446, Faculte de Pharmacie, Universite Paris-Sud, F-92296 Châtenay-Malabry, France. naja.abi-g@cep.u-psud.fr

The Journal of Physiology
|February 17, 2001
PubMed

Insights

Nitric oxide (NO) donors like DEANO inhibit cardiac L-type Ca2+ current (ICa,L) via a cGMP-dependent pathway. This effect involves cGMP-dependent protein kinase activation and a pertussis toxin-sensitive G protein, mediating anti-adrenergic actions.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Pharmacology
  • Cell Signaling

Background:

  • Nitric oxide (NO) plays a crucial role in cardiovascular regulation.
  • The cGMP pathway is implicated in NO signaling.
  • Modulation of cardiac L-type Ca2+ current (ICa,L) affects heart function.

Purpose of the Study:

  • To investigate the role of the cGMP pathway in NO-mediated modulation of cardiac ICa,L in rat ventricular myocytes.
  • To elucidate the specific signaling molecules involved in this NO effect.

Main Methods:

  • Patch-clamp electrophysiology was used to measure ICa,L in rat ventricular myocytes.
  • Various NO donors (DEANO, SIN-1, SNP, SNAP, GSNO) were applied.
  • Inhibitors of NO-sensitive guanylyl cyclase (ODQ) and cGMP-dependent protein kinase (cG-PK) were utilized.
  • Pertussis toxin was used to assess the involvement of G proteins.

Main Results:

  • DEANO inhibited isoprenaline- or IBMX-stimulated ICa,L, but not basal ICa,L.
  • This inhibitory effect of DEANO was dependent on cGMP, as it was antagonized by ODQ and cG-PK inhibitors.
  • The effect was mediated by a pertussis toxin-sensitive G protein.
  • Exogenous cAMP attenuated the inhibitory effect of DEANO.

Conclusions:

  • DEANO exerts anti-adrenergic effects on rat ventricular myocytes.
  • This action is mediated through a cGMP-dependent pathway involving cG-PK activation.
  • A pertussis toxin-sensitive G protein is integral to this NO-induced modulation of ICa,L.

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