Binge drinking affects kidney function, osmotic balance, aldosterone levels, and arterial pressure in adolescent rats: the potential hypotensive effect of selenium mediated by improvements in oxidative balance.

Binge drinking (BD) during adolescence is related to hypertension. There are, however, few studies concerning the effects of BD on kidney function and osmotic balance in relation to arterial pressure. The mechanism by which BD affects kidney function is related to oxidation and inflammation. Recently, Se, an essential trace element possessing antioxidant properties, has also been shown to be related to renal Na+ /K+ -ATPase activity. This study examined the protective effects of 0.4 ppm selenite administered to adolescent rats in an intermittent i.p. BD model. BD consumption depleted kidney and serum Se deposits, decreased GPx activity, and increased biomolecule oxidation in these locations. In the kidneys, GPx1, GPx3, GPx4, and NF-κB expression also decreased, coinciding with an increase in caspase-3 expression. BD decreased creatinine clearance and fractional Na+ excretion (EFNa), increased transtubular K+ excretion (TTKG) and serum aldosterone (Aldo) levels, and reduced relative Aldo clearance. These effects led to hypernatremia, low urinary flow, and high systolic blood pressure. Se supplementation to BD rats significantly improved oxidative balance, and kidney GPx, NF-κB, and caspase-3 expression; slightly increased EFNa and slightly decreased TTKG and serum Aldo levels; and greatly increased relative Aldo clearance. Se supplementation did not, however, modify creatinine clearance. In conclusion, BD triggers kidney osmotic and ionic imbalances, which contribute to increasing systolic blood pressure. These disturbances could be related in part to Se and selenoprotein GPxs, which decrease oxidative, inflammatory and apoptotic alterations in the kidneys. Se supplementation prevents these changes, improves ionic disturbances, and decreases serum Aldo levels and systolic blood pressure.