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Increased Norepinephrine Breakdown Adverse for Heart

Generation of reactive oxygen species contributes to adverse cardiac remodeling

THURSDAY, Jan. 14 (HealthDay News) -- Increased norepinephrine levels due to cardiac stress lead to greater norepinephrine breakdown, generating reactive oxygen species that contribute to adverse cardiac remodeling and dysfunction, according to a study in the Jan. 8 issue of Circulation Research.

Nina Kaludercic, Ph.D., from the Johns Hopkins School of Medicine in Baltimore, and colleagues examined the effect of norepinephrine on monoamine oxidase-A (MAO-A), which metabolizes norepinephrine and generates reactive oxygen species, in myocytes and in mice with cardiac remodeling due to pressure overload.

The researchers found that MAO-A activity was induced in myocytes after norepinephrine stimulation, accompanied by increases in cell size, production of reactive oxygen species, and signs of maladaptive hypertrophy. In mice with maladaptive remodeling (left ventricular hypertrophy, dilation and pump failure) due to pressure overload, greater norepinephrine breakdown was accompanied by increased oxidative stress. These changes were blocked by an MAO-A inhibitor, and mice engineered to have blocked MAO-A function were better protected from the adverse effects of pressure overload.

"In addition to adrenergic receptor-dependent mechanisms, enhanced MAO-A activity coupled with increased intramyocardial norepinephrine availability results in increased reactive oxygen species generation, contributing to maladaptive remodeling and left ventricular dysfunction in hearts subjected to chronic stress," Kaludercic and colleagues conclude.

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