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Significance ATP-sensitive potassium (KATP ) channels are present in cardiac and smooth muscle; when activated, they relax blood vessels and decrease cardiac action potential duration, reducing cardiac contractility. Cantu syndrome (CS) is caused by mutations in KATP genes that result in overactive channels. Contrary to prediction, we show that the myocardium in both CS patients and in animal models with overactive KATP channels is hypercontractile. We also show that this results from a compensatory increase in calcium channel activity, paralleled by specific alterations in phosphorylation of the calcium channel itself. These findings have implications for the way the heart compensates for decreased excitability and volume load in general and for the basis of, and potential therapies for, CS specifically.

K ATP channel gain-of-function leads to increased myocardial L-type Ca 2+ current and contractility in Cantu syndrome

K _ATP channel gain-of-function leads to increased myocardial L-type Ca ²⁺ current and contractility in Cantu syndrome