AT1-receptor blockade in experimental myocardial ischemia/reperfusion.
The renin-angiotensin system is activated during myocardial ischemia, and angiotensin II is locally formed in ischemic hearts. At least four angiotensin II receptor subtypes have been identified, the AT1- and the AT2-receptor being the most prominent in the cardiovascular system. AT1-receptor blockade--like inhibition of the angiotensin-converting-enzyme (ACE)--limits infarct size, improves functional recovery following myocardial ischemia and attenuates ventricular remodeling, post-myocardial infarction and the resulting development of heart failure. The potential mechanisms responsible for the cardioprotection by AT1-receptor blockade remain to be elucidated in detail, but appear to involve AT2-receptor activation and--like ACE-inhibitors--bradykinin and prostaglandins. Combined treatment with ACE-inhibitors and AT1-receptor blockers has the potential to further reduce infarct size and improve ventricular remodeling over each monotherapy alone.
Schulz
R
R
Institute for Pathophysiology, Center for Internal Medicine of the University Hospital, Essen, Germany. rainer_schulz@uni-essen.de
Heusch
G
G
D047228:Angiotensin II Type 1 Receptor Blockers; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D004195:Disease Models, Animal; D017202:Myocardial Ischemia / Q000188:drug therapy*; D044140:Receptor, Angiotensin, Type 1 / Q000627:therapeutic use*
D047228:Angiotensin II Type 1 Receptor Blockers; D044140:Receptor, Angiotensin, Type 1