Redox Regulation of Circulating NO Bioavailability

Abstract

PURPOSE: The present study sought to determine free radical-mediated regulation of circulating Nitric Oxide (NO) bioavailability during a sustained period of post-exercise hypotension (PEH) in hypertensive men. METHODS: Nine borderline hypertensive males, MAP = 106 ± 5 mmHg (50 ± 10 yr), not on medication, were studied following 30-minutes of cycle exercise at 70% maximal oxygen consumption. The subjects were followed post-exercise for 2-hours. Peripheral venous blood was sampled from an antecubital vein pre-, immediately post-, 1-hour post- (P1) and 2-hours post- (P2) exercise and corrected for plasma volume shifts. Plasma nitrate/nitrite was determined utilising a fluorometric assay, whilst S-Nitrosothiol (RSNO) concentrations were assayed by the Saville reaction and ELISA technique. Indirect markers of free radical generation were determined via the FOX1 assay detecting lipid hydroperoxides (LHP). RESULTS: Exercise decreased systemic mean arterial pressure by ∼5mmHg and elevated LHP (Table 1) whereas exercise failed to modify nitrite or RSNO concentration. However nitrate fell significantly below baseline following exercise.Table 1: Blood Pressure and Metabolic Responses to Sub-maximal Cycle ExerciseCONCLUSION: The results of the present study indicate that despite increases in oxidative stress circulating markers of NO bioavailability had no effect on the observed hypotension. An intriguing antagonism exists whereby elevated oxidative stress reduces the bioavailability of NO but a sustained hypotension remains. This suggests that PEH is resultant from a metabolic pathway independent of NO.