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Irbesartan-mediated AT1 receptor blockade attenuates hyposmotic-induced enhancement of I Ks current and prevents shortening of action potential duration in atrial myocytes.
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Abstract
Stretch of the atrial membrane upregulates the slow component of delayed rectifier K(+) current (I(Ks)). Blockade of angiotensin II subtype 1 receptors (AT(1)R) attenuates this increase in I(Ks). The present study aimed to examine the effects of irbesartan, a selective AT(1)R blocker (ABR), on both the enhancement of I(Ks) and the shortening of action potential duration (APD) induced by stretching atrial myocytes for exploring the mechanisms underlying the prevention of atrial fibrillation (AF) by ABR.