We showed that sympathetic hyperactivity does not change VEGF and Akt, which is a key intracellular mediator of this pathway. However, our findings are in accordance with lines of evidence showing that exercise induces a local angiogenic phenotype characterized by overexpression of VEGF in the heart. Moreover, we observed high expression of active Akt form and Bcl-2 protein as well as a SCH772984 reduction of pro-apoptotic Bad. These findings have been previously shown in myocardial injury by ischemia/reperfusion, hypertension, and diabetes. Thus, as a novel finding, we show that the kallikrein-kinin system/VEGF/Akt pathway may be involved in exercise-induced cardioprotection against sympathetic hyperactivity. In the current study, one cardioprotective pathway elicited for kinin and VEGF action could be NO release. NO is a short-lived free radical gas involved in several physiological and pathological processes. When synthesized by eNOS, NO plays an important role in endothelial function and cardioprotection. In fact, findings have emphasized that NO may antagonize sympathetic stimulation. Therefore, our findings showed an increase of eNOS in exercise rats, suggesting that this molecule may participate in cytoprotection from the cardiotoxic effects of catecholamines. Preterm birth, respiratory distress syndrome, and bronchopulmonary dysplasia, the chronic lung disease of prematurity, continue to be important causes of morbidity and mortality in the neonatal intensive care unit. Despite improvements in perinatal care, the incidence of BPD remains unchanged. Preterm birth before 28 weeks of gestation interrupts the normal sequence of lung growth leading to impaired alveolar and lung vascular development. Emerging evidence suggests that BPD may have long-term respiratory complications that reach beyond childhood. Follow-up studies indicate that children and young adults who were born very preterm are at an increased risk of respiratory symptoms, poor lung function, lower exercise capacity and pulmonary hypertension. Currently, there is no effective treatment for BPD. Hydrogen sulfide has long been considered a noxious and toxic gas. Newly acquired evidence indicates potential biomedical applications for H2S. H2S is now recognized – along with carbon monoxide and nitric oxide – as an endogenous gaseous mediator exerting important physiological actions. The role of H2S in the developing lung is unknown. The discovery that H2S is an endogenously produced gaseous second messenger capable of modulating many physiological processes including vasodilation and cytoprotection, much like NO, prompted us to investigate the potential of H2S as a lung-protective agent. Thus, we hypothesized that H2S would preserve alveolar development and prevents PHT in experimental oxygen-induced lung injury in newborn rats. Our findings demonstrate the protective effect of H2S on chronic hyperoxia-induced injury in the developing lung: In vitro, treatment with H2S protects HPAECs from O2 toxicity and promotes HPAECs network formation. In vivo, H2S administration preserves and restores alveolar growth and alleviates echographic and structural signs of PHT.