Impact of circulating angiotensin II concentration on redox regulation of post-exercise haemodynamics

We previously reported that a single bout of dynamic exercise induces a sustained post-exercise vasodilatation independent of enhanced circulating NO bioavailability (New et al, 2008). Recent evidence however points to reactive oxygen species as important mediators of angiotensin II (ANG II) induced vascular dysfunction (Pena-Silver and Heistad, 2010). The present study therefore investigated the influence of exercise-induced increases in ANG II on circulating biomarkers of oxidative stress and concomitant post-exercise haemodynamics. 9 older males, MAP = 106 ? 5 mmHg (50 ? 10 yr), not on medication, were studied following 30-minutes of cycle exercise at 70% maximal oxygen consumption. Subjects were followed post-exercise for 2-hours. Left ventricular haemodynamics were assessed via echocardiography and systemic vascular resistance (SVR)/vascular conductance (SVC) determined by the quotient of MAP/Q and Q/MAP, respectively. Peripheral venous blood was sampled from an antecubital vein pre-, immediately post-, 1-hour post- (P1) and 2-hours post- (P2) exercise and metabolite concentrations corrected for plasma volume shifts. ANG ?? concentrations were determined in venous plasma, following an extraction procedure, via a double-antibody radioimmunoassay. Indirect markers of oxidative stress were determined spectrophotometrically detecting lipid hydroperoxides (LOOH) whilst blood was also assayed for selective antioxidants by HPLC. Data were analysed with a repeated measures ANOVA and post-hoc Bonferroni-corrected paired samples T-tests. Exercise decreased SVR whilst concomitantly elevating ANG ?? and LOOH concentration (Table 1) (Pandlt;0.05; Paired samples T-tests). The lowered systemic vascular resistance post-exercise transcended into a mean arterial pressure reduction of ~5mmHg (Pandlt;0.05; Paired samples T-tests). These results indicate that attenuated vascular resistance following exercise occurs despite increases in ANG II and oxidative stress and that increased oxidative stress follows elevated ANG II. A profound vasodilatory mechanism capable of buffering powerful vasoconstriction exists mediating the exercise-induced hyperaemia.