Volume 2, Number 1, March 2001

AT₁-receptor blockade in experimental myocardial ischaemia/reperfusion
Rainer Schulz, Gerd Heusch

The renin-angiotensin-aldosterone system (RAAS) is activated during myocardial ischaemia, and angiotensin II (Ang II) is formed locally in ischaemic hearts. At least two Ang II receptor subtypes, the AT₁- and the AT₂-receptor, have been identified. AT₁-receptor blockade, like angiotensin-converting enzyme (ACE) inhibition, limits infarct size, improves functional recovery following myocardial ischaemia and attenuates ventricular remodelling post-myocardial infarction (MI) 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 (ACE-I), bradykinin potentiation. Combined treatment with ACE-I and AT₁-receptor blockers reduces infarct size and improves fractional shortening of myocytes from failing hearts more than either monotherapy alone.

JRAAS 2001;2:136-140.

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