Background. The high mortality rate among patients with acute myocardial infarction (AMI) is an important problem of modern cardiology. In recent years, there has not been a significant decrease in mortality in AMI. Drugs used to treat AMI are not effective enough, so there is a need to develop fundamentally new drugs that can significantly increase the heart’s tolerance to ischemia/reperfusion (I/R). Angiotensin 1-7 peptide, which can increase cardiac tolerance to I/R by activating Mas receptor in myocardial tissue, could become a prototype of such drugs. The following enzymes are involved in the formation of the cardioprotective effect of angiotensin 1-7: NO-synthase, soluble guanylyl cyclase, phosphoinositide 3-kinase, extracellular signal-regulated kinases-1/2, Akt kinase and, possibly, protein kinase G. Indirect data indicate that the hypothetical end effector in the cardioprotective impact of angiotensin 1-7 could be mitochondrial or sarcolemmal ATP-sensitive K+ channel.Aim: To review 1-7 role in increasing the heart resistance to ischemia and reperfusion. The literature search was carried out in the PubMed database with queries “angiotensin 1-7 receptors”, “stress”, “angiotensin 1-7”, “mas receptor”, “cardioprotective effects of angiotensin 1-7”.