NITRIC OXIDE SYSTEM INHIBITION MODIFIES CARDIAC AQP1 LOCALIZATION DURING HYPOVOLEMIC STATE IN GROWING RATS

VANINA NETTI; A. IOVANE; M. VATRELLA; ELSA ZOTTA; , ANDREA FELLET; ANA MARÍA BALASZCZUK

Atenas

Congreso; 24 European Meeting on Hypertension; 2014

Abstract We showed an age-related regulation of cardiac AQP1 in response to dehydration during postnatal growth. AQP1 may transport nitric oxide (NO) in endothelial cells. The aim of the present work is to study if NO system inhibition regulates cardiac AQP1 during dehydration in growing rats. Methods: Male Sprague-Dawley rats aged 25 and 50 days (n=8): R: water restriction 3 days; C: water ad libitum 3 days; RL: infusion of NO synthase (NOS) inhibitor L-NAME (4mg/kg.day) via osmotic mini pumps + water restriction 3 days; CL: L-NAME (4mg/kg.day) + water ad libitum 3 days. NOS activity and AQP1 protein levels and localization were determined. Results: L-NAME treatment decreased NOS activity in CL and RL groups of both ages; NOS activity was increased in R25 pups but not in R50. AQP1 immunohistochemical staining of the heart revealed its presence in vascular endothelium and endocardium in C and CL animals of both ages. Cardiac AQP1 levels were increased in R50 and RL50 and appeared in cardiomyocyte membrane. L-NAME treatment also decreased ventricular AQP1 in CL50. No changes in AQP1 protein levels or localization were observed in the R25, but RL25 group also showed AQP1 presence on the membrane. Conclusion: Cardiac NO system and AQP1 abundance and localization during osmotic stress depend on postnatal age. Age-related influence of NO system inhibition on AQP1 protein levels and localization in the heart probably affects cardiac water homeostasis during hypovolemic state.