CONICET | Buscador de Institutos y Recursos Humanos

Objective: We previously showed changes in cardiac AQP1 protein levels and localization during water restriction according to the stage of postnatal growth studied. It has been reported that AQP1 transports nitric oxide (NO) out of endothelial cells and into vascular smooth muscle. The objective of the present work is to study if NO system inhibition regulates cardiac AQP1 protein levels in vivo during dehydration in postnatal stages. Design and method: Male Sprague-Dawley rats aged 25 and 50 days were randomly assigned as follows (n=7): R: water restriction 3 days; C: water ad libitum 3 days; RL: infusion of NO synthase (NOS) inhibitor L-NAME (4mg/kg.day) via ALZET osmotic mini pumps + water restriction 3 days; CL: L-NAME (4mg/kg.day) + water ad libitum 3 days. NOS activity to verify NO system inhibition ([14C] L-Arginine) and AQP1 protein levels (Western Blot) were determined in the left ventricle and right atria. Results: L-NAME treatment decreased NOS activity in CL and RL groups of both ages by 50%, each compared to their control group. NOS activity was increased in R25 pups and not in R50. Left ventricular AQP1 protein levels were increased in R50, without changes in dehydrated pups. L-NAME treatment decreased ventricular AQP1 in CL50 and increased in RL50 similar to R50 group, without changes in L-NAME-treated pups. In the right atrium, no changes were observed in AQP1 in response to water restriction in both age groups. However, CL25 group had decreased levels of this water channel and increased in RL25 compared to CL25. In the 50-day-old group, CL50 group had similar levels of AQP1 to C50, but RL50 presented higher AQP1 protein levels compared to R50. Conclusion: NO system activity and AQP1 protein levels in cardiac tissue during osmotic stress depend on postnatal age. NO system inhibition influences AQP1 protein levels in the heart, probably affecting its diffusion across the plasma membrane.