Brief periods (a few seconds) of cyclic
coronary occlusions applied early in reperfusion induce a cardioprotection against
infarct size, called postconditioning (PostC) in which B(2)-bradykinin receptors play a pivotal role. Since
angiotensin-converting enzyme (
ACE) inhibitors reduce degradation of
kinins, we studied the effects of PostC on
infarct size and postischemic myocardial dysfunction in both normotensive (WKY) and spontaneously hypertensive rats (SHR) acutely or chronically treated with the
ACE inhibitor Captopril. Isolated hearts from SHR and WKY rats were subjected to the following protocols: (a)
ischemia for 30- and 120-min reperfusion (I/R); (b) I/R + PostC protocol (5-cycles 10-s I/R); (c) pretreatment with
Captopril for 4-weeks before to subject the hearts to I/R with or without PostC maneuvers. Some SHR hearts were treated with
Captopril during the 20- or 40-min early reperfusion with or without PostC maneuvers. Cardiac function was assessed in vivo with echocardiography. Left ventricular pressure and
infarct size were measured ex vivo. Chronic
Captopril significantly reduced
left ventricular hypertrophy in SHR, and reduced
infarct size in both WKY and SHR hearts. PostC maneuvers significantly reduced
infarct size in WKY, but not in SHR hearts. Yet, PostC slightly improved postischemic systolic function in untreated SHR.
Captopril given in reperfusion was unable to limit I/R injury in SHR hearts. Data show that PostC protection against
infarct size is blunted in SHR and that PostC is unable to add its protective effect to those of chronic
Captopril, which per se reduces
cardiac hypertrophy and heart susceptibility to I/R insult.