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Vol. 300, Issue 2, 681-687, February 2002
Department of Cardiac Physiology, National Cardiovascular Center
Research Institute, Osaka, Japan
Acetylcholine causes bradycardia through M2 muscarinic receptors in
sinoatrial node cells. I examined with electrocardiogram how the
muscarinic K+ (KACh) channel participates in
the sinus bradycardia induced by a muscarinic agonist in the
Langendorff preparation of rabbit hearts. In the presence of 100 nM
propranolol, 1 nM to 10 µM carbachol (CCh) induced sinus bradycardia
in a concentration-dependent manner. Tertiapin (100 or 300 nM), which
selectively blocks KACh channels in cardiac myocytes,
significantly inhibited the effect of 
300 nM but not 
100 nM CCh.
The effect of CCh was divided into tertiapin-sensitive and -insensitive
components. The former component was induced by >100 nM CCh in a
concentration-dependent manner and accounted for ~75% of the maximum
effect of CCh. The KACh channel in atrial myocytes was also
activated by this range of concentrations of CCh as measured with the
patch-clamp method. The tertiapin-insensitive component was induced by
1 to 300 nM CCh in a concentration-dependent manner and accounted for
~25% of the maximum effect of CCh. The sinus rate in the presence of
1 µM CCh and 300 nM tertiapin was similar to that in the presence of
2 mM CsCl, a blocker of the hyperpolarization-activated
If current. Furthermore, no
tertiapin-insensitive component existed in the presence of 2 mM CsCl.
Therefore, the negative chronotropic effect of 300 nM CCh is mainly
mediated by KACh channels, whereas that of 100 nM CCh may
result from suppression of the If current.
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