Angiotensin II Potentiates the Slow Component of Delayed Rectifier K⁺Current via the AT₁Receptor in Guinea Pig Atrial Myocytes

Abstract

The potentiation of IKs via AT1 stimulation in atrial myocytes, accompanied by a shortening of the action potential duration, suggests a potential mechanism by which elevated levels of Ang II may promote atrial fibrillation in heart failure and warrants further investigation.