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Acta Physiologica 2007; Volume 189, Supplement 653
The 86th Annual Meeting of The German Physiological Society
3/25/2007-3/28/2007
Hannover, Germany
ALTERATIONS OF BASAL ENOS-ACTIVATION IN HUMAN FAILING MYOCARDIUM
Abstract number: O14-2
Napp1 A, Brixius1 K, Mehlhorn1 U, Schwinger1 RHG, Bloch1 W
1Institute of Cardiovascular Research, and Sport Medicine, Dept. of Molecular and, Cellular Sport Medicine, Cologne
There is evidence from few publications that eNOS-activation is altered in failing myocardium. However, the mechanisms underlying eNOS-activation are complex and have not yet been investigated in human endstage heart faiure.
Therefore, we performed Western blot experiments and immunohistochemical stainings of the eNOS-protein, eNOS- translocation and ?phosphorylation (serine 1177, threonine 495, serine 114, serine 635) in left ventricular myocardium from human non-failing (NF, donor hearts, n=6) and failing hearts (dilated cardiomyopathy, DCM, orthotopic heart transplantations, AHA/ESC stadium D, n=12).
ENOS-protein expression was similar in NF and DCM. In addition, eNOS-translocation and Thr495-phosphorylation were unchanged in DCM compared to NF. ENOS-phosphorylation was decreased at serine 1177 and Ser114 but increased at Ser635. These alterations were going along with an increase in oxidative and nitrosative free radical production.
In conclusion, due to the alterations in basal eNOS activation mechanisms, cardiac NO-liberation seems to be decreased in human heart failure. This may contribute to a decreased defense against cellular apoptosis.
To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 189, Supplement 653 :O14-2