Aging induces deleterious effects in several organs, and is associated with complex changes in cardiovascular structure and function. This process might be due to damage caused by inflammatory mediators, free radicals and apoptosis (1-3). The purpose of this study was to investigate the effect of aging on different parameters related to apoptosis and NFkB (nuclear factor kappa B) expression in hearts from male senescence-accelerated mice (SAM-P8) and its controls male senescence-accelerated-resistant (SAM-R1). Also to study the influence of chronic administration of Growth Hormone (GH) on these parameters in old SAM-P8 mice. Forty male mice were used. Animals were divided into five experimental groups, two old groups of 10 month of age (SAM-P8/SAM-R1), one GH group of also 10 months age (SAM-P8), that was treated with the hormone (2 mg/kg/day/s.c.) and two young groups, of 2 months of age (SAM-P8/SAM-R1) that were used as young controls. After 30 days of treatment, animals were sacrificed by decapitation, and hearts were collected. The expression of BCL2-associated death promoter (BAD), BCL2-associated X protein (BAX), B-cell lymphoma 2 (BCL2) and NFkB, were determined by real-time reverse transcription polymerase chain reaction. Results were submitted to a two way ANOVA statistical evaluation using the Statgraphics program. The expression of NFkB (p<0.05) and BAX (p<0.01) were significantly increased in the old SAMP-8 control males, as compared to young mice. Age also diminished the levels of BCL2 (p<0.01), in this animals. In the case of SAM-R1 animals a significantly increased BAX as found (p<0.05), as compared to SAM-R1 young controls. The expressions of NFkB and BCL2 were similar in old and young SAM-R1 mice. The expression of BAD on SAM-P8 and SAM-R1 mice, showed no significant differences between young and old animals. Exogenous GH administration showed a significant decrease in levels of NFkB (p<0.01), BAX (p<0.01) and BAD (p<0.05). The expression of BCL2 was not significantly affected with the treatment in old SAM-P8. Our results suggest that the inflammatory process and some mediators of apoptosis could contribute to the observed alterations of the cardiovascular system associated with aging and that GH may play a potential protective effect during this process.