The study shows that the reduction in myocardial Cx43 content 2 weeks after cardiac infarction is less in iNOS−/− than in wild-type (WT) mice. Moreover, iNOS deficiency preserves the ratio of the phosphorylated to nonphosphorylated Cx43, improves cardiac function and increases survival. Finally, in vitro experiments demonstrate that exogenous NO production dose-dependently decreases Cx43 content in isolated cardiomyocytes.