Journal article
Combination renin-angiotensin system blockade and angiotensin-converting enzyme 2 in experimental myocardial infarction: Implications for future therapeutic directions
LJ Burchill, E Velkoska, RG Dean, K Griggs, SK Patel, LM Burrell
Clinical Science | PORTLAND PRESS LTD | Published : 2012
DOI: 10.1042/CS20120162
Abstract
The RAS (renin-angiotensin system) is activated after MI (myocardial infarction), and RAS blockade with ACEis [ACE (angiotensin-converting enzyme) inhibitors] or ARBs (angiotensin receptor blockers) slows but does not completely prevent progression to heart failure. Cardiac ACE is increased after MI and leads to the formation of the vasoconstrictor AngII (angiotensin II). The enzyme ACE2 is also activated after MI and degrades AngII to generate the vasodilator Ang-(1-7) [angiotensin-(1-7)]. Overexpression of ACE2 offers cardioprotective effects in experimental MI, but there is conflicting evidence as to whether the benefits of ACEis and ARBs are mediated through increasing ACE2 after MI. In ..
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Funding Acknowledgements
This work was partially funded by grants from the National Heart Foundation of Australia and the National Health and Medical Research Council of Australia. L.M.B. was the recipient of a National Heart Foundation Scholarship (Melbourne, Victoria, Australia) and a postgraduate student scholarship from the University of Melbourne.