ACE2 / (MLNM)
NEW YORK (Reuters Health) - Scientists are zeroing in on the function of a recently discovered enzyme, ACE2, that appears to be an important player in normal heart function, according to the results of a new study in rodents.
Dr. Josef M. Penninger of the University of Toronto in Canada, said ACE2 appears to be "the good guy" that protects the heart and cardiovascular system.
ACE2, which was discovered 2 years ago, is similar to a previously known enzyme, ACE. ACE contributes to high blood pressure, or hypertension, by constricting blood vessels. Blocking the enzyme with ACE inhibitors can lower pressure and help ease congestive heart failure, a condition in which the heart pumps blood inefficiently and results in fatigue and fluid build-up in the limbs and lungs.
Now, researchers are reporting in the June 20th issue of the journal Nature that ACE2--which is found only in the heart, kidneys and testes--may also help regulate blood pressure.
In the new study, the researchers studied rats with high blood pressure as well as looked for the location of the gene that produces ACE2. The team then created genetically engineered mice that lacked the ACE2 gene, the ACE gene, or both genes.
"The hope was that inhibition of ACE2 might provide a new drug target for hypertension," said Penninger. "Instead, we found something completely unexpected and novel--ACE2 is a major protein that controls how the heart functions, and in the absence of ACE2, mutant mice develop heart failure."
However, mice that lacked both ACE and ACE2 did not develop heart failure, suggesting that ACE is responsible for the declining heart function and that ACE2 counteracts the function of ACE.
What's more, the mice that lack ACE2 share similarities with humans with heart disease, Penninger said.
"Thus, we have a mouse model that we can use to develop novel drugs, and of course finding out how things work we can selectively interfere with heart and cardiovascular diseases," he told Reuters Health.
"The nice thing is that ACE2 is very specific for the heart and so we could design drugs with minimal side effects in other organs," he added. "After all, heart diseases are the major killer in this world," he added.
SOURCE: Nature 2002;417:822-827.
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