[Acetylcholine and the myocardium: electrophysiological aspects].
The cardiac inhibitory effects (negative inotropic and chronotropic) of muscarinic cholinergic stimulation by acetylcholine (ACh) are well established. They are due to electrophysiological modifications involving (1) the activation of the resting K+ channel showing inward going rectification properties; (2) the reduction of the inward calcium current (I Ca). Recent works on isolated myocardial cells allowed to investigate the molecular mechanisms involved between muscarinic cholinergic receptors activation and effector (the ionic channel). The results indicate that muscarinic receptor communicates with the K+ channel, via GTP-binding protein (Ni, o or G) and that does not involve adenylate-cyclase. In contrast to the direct muscarinic activation of K+ channel, ACh decreases I Ca by inhibiting, via Ni, the cAMP production. The inhibition of I Ca is larger in the beta-stimulated cells.
Garnier
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Laboratoire d'Electrophysiologie et Pharmacologie Cellulaires, Faculté des Sciences et Techniques, Tours, France.
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D015220:Calcium Channels / Q000502:physiology; D004553:Electric Conductivity; D004594:Electrophysiology; D019204:GTP-Binding Proteins / Q000502:physiology; D006321:Heart / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D011976:Receptors, Muscarinic / Q000502:physiology
D015220:Calcium Channels; D015221:Potassium Channels; D011976:Receptors, Muscarinic; D019204:GTP-Binding Proteins; D000109:Acetylcholine
L'acétylcholine et le myocarde: aspects électrophysiologiques.