Modulation of cardiac remodeling by adenosine: in vitro and in vivo effects.
The increasing incidence of congestive heart failure has stimulated efforts to develop pharmacologic strategies to prevent or reverse the associated process of adverse cardiac remodeling. The possibility of utilizing endogenously generated factors that are capable of inhibiting this process is beginning to be explored. Adenosine, has been described as a retaliatory autacoid with homeostatic activities in the regulation of myocardial blood flow, catecholamine release, and reduction of injury resulting from periods of ischemia. Adenosine exerts a variety of actions that are consistent with the concept that it can reduce or inhibit the process of cardiac remodeling. In this manuscript, the basics of adenosine metabolism, its cell surface receptors and beneficial actions on the cardiovascular system are reviewed. In addition new, in vitro and in vivo data will be presented supporting the concept that adenosine exerts actions that may ameliorate adverse cardiac remodeling.
Department of Medicine, University of California, San Diego 92103-8412, USA. fvillarr@ucsd.edu
Francisco
F
Villarreal
Scott
S
Zimmermann
Lala
L
Makhsudova
Annika C
AC
Montag
Mark D
MD
Erion
David A
DA
Bullough
Bruce R
BR
Ito
D000241:Adenosine / Q000378:metabolism* / Q000627:therapeutic use*; D000818:Animals; D002319:Cardiovascular System / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D008954:Models, Biological; D009203:Myocardial Infarction / Q000188:drug therapy*; D017202:Myocardial Ischemia / Q000188:drug therapy; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D018047:Receptors, Purinergic P1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology*
D018047:Receptors, Purinergic P1; D014409:Tumor Necrosis Factor-alpha; D000241:Adenosine