CATECHOLAMINES AND THEIR METABOLITES IN REGULATION OF HEART ENZYMS

Abstract

Currently in cardiology it is important establish mechanisms of adaptation disorder processes observed during hyperactivity sympathetic nervous system, to develop adequate methods of treating cardiovascular diseases. By nature, sympathetic hyperactivation is accompanied by increased formation of enzymatic and non-enzymatic products enzymatic metabolism of catecholamines, which can change the activity of mitochondrial and cytosolic enzymes, contributing to changes in the level bioenergetic adaptation, antioxidant systemprotection and synthesis of intercellular modulators, such as AMP and adenosine [1]. It is known that catecholamines adrenaline and norepinephrine increases blood glucose levels by stimulating glycogenolysis and gluconeogenesis by activation of β- and α-receptors of hepatocytes, through enhancing glucagon secretion and by inhibiting insulin-mediated glucose uptake into muscle and adipose tissue. Adrenaline activates lipase adipose tissue, increasing the level of free fat acids that undergo β-oxidation in mitochondria. Adrenaline increases the speed of the main metabolism with a subsequent increase in thermogenesis, induces mitochondrial biogenesis and increases aerobic capacity of tissues, changing the content mitochondrial proteins. Causes an increase release of H2O2 and other reactive oxygen species due to stimulation of mitochondrial respiration during simultaneous decrease in the activity of antioxidants enzymes [2]. Active forms in living systems oxygen play a dual role - they can cause oxidative damage and tissue dysfunction and serve as molecular signals that activate stress reactions. Mitochondria, thanks to their ability to produce free forms oxygen, play an important role in oxidative tissue damage, while at the same time providing protection against excessive tissue dysfunction [5].