PP.25.06

Objective: Renal vasodilatation during L-arginine (ARG) infusion is impaired in essential hypertensive (HTN) vs. healthy (C) humans. Whether or not different ARG effects on the oxidative stress (OS) do participate in such abnormal responses is not known. Design and method: Mean arterial pressure (MAP), glomerular filtration rate (GFR, inulin), renal blood flow (RBF, p-aminohippurate), and urinary excretion of sodium (UNaV), NO2+NO3 (UNOxV), and 8-isoprostane (U8-iso-PGF2alfaV) were measured in 16 salt-repleted C and 19 HTN undergoing 3-hours infusion of 0.012 mmol.kg.min-1 ARG.HCl. Results: In contrast to the markedly decreased U8-iso-PGF2alfaV with ARG.HCl in C, in HTN a slightly increased U8-iso-PGF2alfaV is associated with impaired renal vasodilatation. Therefore, a net reduction in the baseline OS related to the augmented NO bioavailability likely participates physiologically in renal responses to ARG.HCl. In HTN, a limited or abolished capacity of ARG.HCl to affect baseline OS, consistent with impaired scavenging of Reactive Oxygen Species by NO and/or increased formation of peroxynitrite from NO, could contribute to the reduced renal hemodynamic response. Conclusions: In contrast to the markedly decreased U8-iso-PGF2alfaV with ARG.HCl in C, in HTN a slightly increased U8-iso-PGF2alfaV is associated with impaired renal vasodilatation. Therefore, a net reduction in the baseline OS related to the augmented NO bioavailability likely participates physiologically in renal responses to ARG.HCl. In HTN, a limited or abolished capacity of ARG.HCl to affect baseline OS, consistent with impaired scavenging of Reactive Oxygen Species by NO and/or increased formation of peroxynitrite from NO, could contribute to the reduced renal hemodynamic response.