Key result
Kir3.1 knock-out mice exhibited a loss of carbachol-induced current in atrial myocytes, mild resting tachycardias, and blunted responses to pharmacological activation of IKACh.
Population
Kir3.1 knock-out mice and Kir3.4 knock-out mice
Design
Preclinical
Authors
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Should not change practice; confirms Kir3.1 essentiality for IKACh with minimal Kir3.4 contribution in mice.
The Kir3.1 subunit is essential for the function of the muscarinic-gated atrial potassium channel (IKACh), whereas Kir3.4 homomultimers do not significantly contribute to this current.
Bettahi et al. (2002) studied this question. Kir3.1 knock-out vs. Wild-type mice was evaluated on Channel activity and heart rate response. Kir3.1 knock-out mice exhibited a loss of carbachol-induced current in atrial myocytes, mild resting tachycardias, and blunted responses to pharmacological activation of IKACh.
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