Population
Kir6.2-deficient mice and Kir6.2 mice, including ventricular cells, neonatal ventricular cells, aortas, and…
Comparison
Pharmacological K channel openers and gene… vs Wild-type mice/cells and baseline conditions…
Design
Preclinical
Authors
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Kir6.2-dependent cardiac effects of K(+) channel openers may enable selective targeting; leaves open translation to human therapies.
The Kir6.2 subunit mediates the depression of cardiac excitability and contractility induced by K(+) channel openers, but plays no discernible role in the arterial tree.
Masashi Suzuki (2001) studied this question.
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