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Am J Physiol Heart Circ Physiol (April 25, 2002). doi:10.1152/ajpheart.00130.2002
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Articles in PresS, published online ahead of print April 25, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00130.2002
Submitted on February 21, 2002
Accepted on April 12, 2002

Effects of ACh and adenosine mediated by Kir3.1 and Kir3.4 on ferret ventricular cells

H. Dobrzynski1, N. C Janvier1, R. Leach1, J. B Findlay1, and M. R Boyett1*

1 School of Biomedical Sciences, University of Leeds, Leeds, West Yorkshire, United Kingdom

* To whom correspondence should be addressed. E-mail: m.r.boyett{at}leeds.ac.uk.

The inotropic effects of ACh and adenosine on ferret ventricular cells were investigated with the action potential clamp technique. Under current clamp, both agonists resulted in action potential shortening and a decrease in contraction. Under action potential clamp, both agonists failed to decrease contraction substantially. In absence of agonist, application of the short action potential waveform (recorded previously in presence of agonist) also resulted in a decrease in contraction. Under action potential clamp, application of ACh resulted in a Ba2+-sensitive outward current with the characteristics of muscarinic K+ current, iK,ACh - the presence of the muscarinic K+ channel was confirmed by PCR and immunocytochemistry. In absence of agonist, on application of the short ACh action potential waveform, the decrease in contraction was accompanied by loss of inward Na+-Ca2+ exchange current, iNaCa. ACh also inhibited iK,1. It is concluded that ACh activates iK,ACh, inhibits iK,1 and indirectly inhibits iNaCa - this results in action potential shortening, decrease in contraction and, as a result of the inhibition of iK,1, minimum decrease in excitability.




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