Exposure of cardiomyocytes to angiotensin II induces over-activation of monoamine oxidase type A: Implications in heart failure

摘要: Abstract Several evidences indicate that increased cardiac mitochondrial monoamine oxidase type A (MAO-A) activity associates with a failing phenotype. Till now, the mechanism underlying such relation is largely unknown. We explored hypothesis exposure of cardiomyocytes to AT-II caused activation MAO-A and also catalase aldehyde dehydrogenase activities, enzymes involved in degrading MAO's end products. Left ventricular were isolated from normoglycemic (N) streptozotocin-injected (50 mg/kg) rats (D) treated or not losartan (20 mg/kg/day drinking water; DLos NLos, respectively), 1 receptor (AT1) antagonist, for 3 weeks. In each group cells, MAO, activities measured radiochemically spectrophotometrically. The same HL-1 immortalized exposed (100 nM 18 h) absence presence irbesartan (1 μM), an AT1 antagonist. found significantly higher D, than N cells. positively correlated D but over-activation, prevented Similarly, activity, cells acutely this increase was when irbesartan, antagonist present. Over-activation cardiomyocyte among acute (18 h) short-term (2-weeks diabetes) effects novel target antagonists, first line treatments diabetic cardiomyopathy.