The diabetic ischemic heart is resistant to established cardioprotective treatments. The kallikrein-kinin system is involved in myocardial protection from ischemia. However, the respective role of B1 and B2 receptors (B1R and B2R, respectively) remains controversial. The present study tested whether pharmacological activation of kinin receptors may have therapeutic effects in ischemia-reperfusion in normal and diabetic mice. In nondiabetic mice, a B2 agonist reduced infarct size by 47%, but a B1R agonist had no effect. In diabetic mice, the B2R agonist failed to reduce infarct size, but the B1R agonist reduced infarct size by 44%. The differential effect of B2R agonists or B1R agonists in diabetic mice can be linked to inactivation of B2R signaling and induction of B1R in diabetic hearts.
See article at J Pharmacol Exp Ther 2013, 346:23–30.
- Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics