Abstract
Muscarinic K+ channels form a distinct class of cardiac channels, with conductance and kinetic properties that distinguish them from other types of cardiac K+ channels. They are called “muscarinic K+ channels” because they were first identified as the channels responsible for the acetylcholine-induced increase of K+ conductance in cardiac tissue (1). The induction of a K+ conductance increase by acetylcholine (ACh) can be completely blocked by atropine, implying that this action of ACh is mediated by muscarinic receptors. The activation of an inwardly rectifying K+ current is the most prominent cellular response after vagal stimulation or the application of exogeneous ACh in atrial, nodal and Purkinje cells (1–5). The acetylcholine-induced K+ current (i K(ACh)) results in hyperpolarization, decreased rate of spontaneous diastolic depolarization and shortened action potential duration. The K+ conductance increase contributes to the negative chronotropic, negative inotropic and negative dromotropic effect of vagal stimulation. Four other cellular effector pathways further contribute to the cardiac effects of parasympathetic stimulation (for an overview see (6)): 1] antagonism of the production and of the effects of cAMP; 2] stimulation of phosphoinositide turnover; 3] direct reduction of the pacemaker current i f (7); and 4] stimulation of the cellular cGMP content.
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Heidbüchel, H., Carmeliet, E. (1993). Activation Mechanisms of Cardiac Muscarinic K Channels. In: Ostadal, B., Dhalla, N.S. (eds) Heart Function in Health and Disease. Developments in Cardiovascular Medicine, vol 140. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3090-9_4
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DOI: https://doi.org/10.1007/978-1-4615-3090-9_4
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