
Impact of hypoglycemic agents on myocardial ischemic preconditioning
Author(s) -
Rosa Wanda Diez Garcia,
Paulo Cury Rezende,
Whady Hueb
Publication year - 2014
Publication title -
world journal of diabetes
Language(s) - English
Resource type - Journals
ISSN - 1948-9358
DOI - 10.4239/wjd.v5.i3.258
Subject(s) - ischemic preconditioning , medicine , protein kinase c , bradykinin , ischemia , pharmacology , adenosine , signal transduction , neuroscience , microbiology and biotechnology , biology , receptor
Murry et al in 1986 discovered the intrinsic mechanism of profound protection called ischemic preconditioning. The complex cellular signaling cascades underlying this phenomenon remain controversial and are only partially understood. However, evidence suggests that adenosine, released during the initial ischemic insult, activates a variety of G protein-coupled agonists, such as opioids, bradykinin, and catecholamines, resulting in the activation of protein kinases, especially protein kinase C (PKC). This leads to the translocation of PKC from the cytoplasm to the sarcolemma, where it stimulates the opening of the ATP-sensitive K(+) channel, which confers resistance to ischemia. It is known that a range of different hypoglycemic agents that activate the same signaling cascades at various cellular levels can interfere with protection from ischemic preconditioning. This review examines the effects of several hypoglycemic agents on myocardial ischemic preconditioning in animal studies and clinical trials.