Aim: 

PostC depends on B2-bradykinin receptor activation. Since ACE degrades kinins and may desensitize heart B2 receptors, we tested the effects of PostC on infarct size (IS) and postischemic cardiac function in the presence of either acute or chronic ACE-inhibition (ACE-I).

Methods: 

Hearts isolated from spontaneously hypertensive (SHR) and normotensive (WKY) rats were subjected to: a) 30 min ischemia and 120 min reperfusion (I/R), b) I/R + PostC protocol (5 cycles of 10 s I/R at the beginning of R), c) acute ACE-I (Captopril, 200mM) during the 20-40 min early R +/­ PostC; d) chronic ACE-I (300mg/l in drinking water for 4 weeks) before to subject the hearts to I/R +/­ PostC. We assessed left ventricular (LV) end-diastolic and developed pressures, infarct size (IS, % of LV) and LDH release. During chronic ACE-I, LV hypertrophy (LVH) was assessed by echocardiography.

Results: 

IS was smaller in WKY than SHR hearts. PostC limited I/R injury in WKY (IS: 24±3 vs 46±5%, p<0.001), but was less effective in SHR (47±7 vs 70±7%, p< 0.05). Acute ACE-I in R did not alter I/R injury, but progressively limited PostC protection. In SHR, Chronic ACE-I limited LVH (reduced diastolic thickness and systolic thickening of LV); despite LVH regression and a reduced IS by I/R, PostC did not add further protection.

Conclusions: 

PostC protection is reduced in SHR. Acute ACE-I cannot alter I/R injury. However chronic ACE-I reduces LVH and I/R injury, but may alter B2 receptors and blunts PostC protection.