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The effect of carbachol, an analogue of acetylcholine, on the delayed rectifier potassium current, iK, was investigated in rabbit isolated sino-atrial node cells using the whole cell patch clamp technique with amphotericin-permeabilized patches. In the presence of 500 nM atropine and 500 nM hexamethonium to block muscarinic and nicotinic receptors, respectively, 500 nM carbachol decreased the amplitude and rate of deactivation of iK without, however, affecting the slope of the iK activation curve. The same concentration of carbachol decreased the pacemaking rate of spontaneously active sino-atrial node cells by more than 13%. Thus, there is a non-muscarinic and non-nicotinic pathway for cholinergically induced reduction in the amplitude and rate of deactivation of iK that would appear to contribute to negative chronotropy in rabbit sinoatrial node pacemaker cells.

Type

Journal article

Journal

Exp Physiol

Publication Date

07/1999

Volume

84

Pages

631 - 638

Keywords

Amphotericin B, Animals, Atropine, Carbachol, Delayed Rectifier Potassium Channels, Heart Rate, Hexamethonium, In Vitro Techniques, Muscarinic Agonists, Nicotinic Agonists, Patch-Clamp Techniques, Potassium Channels, Potassium Channels, Voltage-Gated, Rabbits, Receptors, Muscarinic, Receptors, Nicotinic, Sinoatrial Node