Abstract

Angiotensin-converting enzyme (ACE) regulates blood pressure and cardiac function by its role in converting the biologically inactive angiotensin I into the vasoconstrictor angiotensin II. The recent discovery of ACE2, a related protease that promotes the generation of vasodilator products from the same precursor, angiotensin I, has raised new questions about the role of the renin–angiotensin system in hypertension and cardiac function. A new study published in Nature compared blood pressure, cardiac function and angiotensin II levels in ACE knockout mice and ACE2 knockout mice. ACE knockout mice had low blood pressure but normal cardiac function, whereas the opposite was observed in ACE2 knockout mice: they displayed normal blood pressure and impaired cardiac contractility. The double knockout (ACE−/−, ACE2−/−) showed a phenotype similar to that of the ACE single knockout, indicating that ablation of ACE rescues the abnormalities in cardiac function induced by the absence of ACE2. [Crackower, M.A. et al. (2002) Nature 417, 822–827] AB

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