Protein Kinase A as Another Mediator of Ischemic Preconditioning Independent of Protein Kinase C

Abstract

Transient preischemic activation of PKA reduces infarct size through Rho-kinase inhibition and actin cytoskeletal deactivation during sustained ischemia, implicating a novel mechanism for cardioprotection by ischemic preconditioning independent of PKC and a potential new therapeutic target.