Keywords: Cardiac hypertrophy; Cerebral arteries; Experiment modeling; NAD; Redox-potential; Tumor necrosis factor alpha; Nuclear factor kappa B IntroductionOne consequence of excessive catecholamine stimulation is an increased β-adrenergic receptor kinase activity leading to uncoupling of the decreased left ventricular myocardial β-adrenoceptor population in failing myocardium. Together with an increase in inhibitory G-proteins, this results in a decreased inotropic responsiveness of the heart to catecholamines. Chronic increased sympathetic activation represents an important hallmark of induced maladaptive (pathologic) hypertrophy development, resulting in myocyte cell death, fibrosis, ventricular dilation, as independent cause of its transition to heart failure [1][2][3][4]. In cardiac hypertrophy (CH) and CHF, the G-dependent pathways activated by norepinephrine, as one of neurohormones, stimulate mitogen-activated protein kinases (MAPK); the elusive signaling pathway responsible for many cerebral and brain injury. Despite of that the common link between CH, endothelial dysfunction, MAPK activation and cerebrovascular events still speculative [5,6]. Several experimental and clinical data suggest that left ventricular (LV) hypertrophy is associated with cerebral damage even in the absence of clinical symptoms [2,3,7]. These hypertrophic stimuli affect the not only a mere response to the mechanical stress from elevated blood pressure, but also dysbalance in some factors (signaling small molecules) promoting the progression of LV pathological remodeling and vasoactive peptides releasing (such as norepinephrine, angiotensin II and endothelin-1), growth factors, oxidative stress markers, heat shock proteins, calcineurin, cytokines and some kinases. Although this diverse array of β-adrenergic stimulated interacting cascades was shown to induce cardiac remodeling, it is not determined yet AbstractBackgrounds: Short-term sustained beta-adrenergic stimulation is a hallmark of sympathetic hyperactivity and a common future in cardiovascular disease. Activation of endogenous cell signaling pathways that negatively regulate cardiac hypertrophy including the decline of NAD and the reduction of the intracellular NAD + /NADH ratio. The hypothesis that prevention of NAD depletion in myocardium may be critical in the treatment of cardiac hypertrophy and inflammatory responses was tested. Methods:On the 7 days of isoproterenol (ISO)-induced cardiac hypertrophy (CH) all animals were randomly assigned into 3 groups: control-without therapy (infusion of 0,9% NaCl); main I-receive 10 mg/kg nebivolol per os in combination with lisinopril infusion; and main II-receive infusion of 15 mg/kg of Nadcin  dissolved in water for injection. All animals were euthanized throughout 7 days after beginning of treatment. Results and conclusion:The increases of heart weight by 18,6% and heart-to-body weight ratio by 35,5% observed in ISO-induced CH were significantly suppressed in lisinopril-nebivolol therapy and monotherapy with NAD + -containi...