Is ACE a new marker for atrial fibrilation?
Sergei M. Danilov1, Viktoria E. Tikhomirova2, Olga V. Kryukova2, Roman A. Serov3, Naida I. Bulaeva3, Leo A. Bokeria3, Olga A. Kost2 and Elena Z. Golukhova3.
1 Department of Anesthesiology, University of Illinois at Chicago, IL
2 Chemistry Faculty, Moscow State University, Russia
3 Bakulev Center for Cardiothoracic Surgery, Moscow, Russia
Background.Angiotensin-converting enzyme (ACE) metabolizes biologically active peptides (AI, BK, Ac-SDKP) and plays a key role in cardiovascular pathologies, including atrial fibrilation (AF). Patients with (AF) are known to have increased level of ACE expression in heart tissues, and, in particular, in atria.
Methodology. We performed ACE phenotyping of postmotem human heart tissues: 1) ACE activity with 2 substrates-ZPHL and HHL; 2) their ratio which allows to detect the presence of endogenous and exogenous ACE inhibitors; 3) degree of ACE inhibition; 3) ACE conformation.
Results. ACE activity in the human heart was 3-fold higher than in the blood and 15-fold lower than in lung. Apparent ACE activity in atria, that was slightly lower than in ventricules, in combination with difference in binding by mAbs to ACE indicates about difference in the levels of endogenous ACE inhibitors/ACE effectors between human atria and ventricules.
Conclusions. We also demonstrated local conformational changes of ACE in different regions of the human heart (atria versus ventricules), that allows us to expect the possibility of generation of mAbs specific to ACE from atria.