Abstract
Increased levels of angiotensin (Ang) II in myocardial infarction (MI), left ventricular (LV) volume overload, and heart failure promote vasoconstriction, increased LV impedance, ischemic injury, ischemia-reperfusion (IR) injury, and LV remodeling with hypertrophy and fibrosis. One strategy for achieving cardioprotection is to decrease Ang II receptor stimulation using angiotensin-converting enzyme (ACE) inhibitors. Another strategy for achieving cardioprotection is by selective blockade of Ang II type 1 (AT1) receptors or type 2 (AT2) receptors using selective antagonists. Functionality has been associated mainly with AT1 receptors, and AT1 receptor blockade is emerging as a new class of agents for therapy of hypertension, LV hypertrophy, and congestive heart failure. The role of AT1 blockade in limiting remodeling after MI has been controversial. Our recent results using the isolated rat working heart model suggest functional roles for both AT1 and AT2 receptor blockade in recovery from IR injury. Furthermore, chronic treatment with AT1 blockade in dogs limited early LV remodeling. Thus, Ang II receptor antagonists are emerging as new cardioprotective agents, alone or in combination with ACE inhibitors.
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