Acute superoxide scavenging reduces sympathetic vasoconstrictor responsiveness in short-term exercise-trained rats.

We hypothesized that acute superoxide (O2(-)) scavenging would attenuate sympathetic vasoconstrictor responsiveness by augmenting nitric oxide (NO)-mediated inhibition of sympathetic vasoconstriction in exercise-trained rats. Sprague-Dawley rats were randomly assigned to sedentary time control (S; n = 7) or mild- (M: 20 m/min, 5° grade; n = 7) or heavy-intensity (H: 40 m/min, 5° grade; n = 7) exercise training (ET) groups and trained 5 days/wk for 4 wk with matched training volume. Following ET, rats were anesthetized and instrumented for lumbar sympathetic chain stimulation and measurement of femoral vascular conductance. In resting skeletal muscle, the percentage change of femoral vascular conductance in response to continuous (2 Hz) and patterned (20 and 40 Hz) sympathetic stimulation was determined during control conditions, O2(-) scavenging (TIRON, 1 g·kg(-1)·h(-1) iv) and combined O2(-) scavenging + nitric oxide synthase blockade (N(ω)-nitro-l-arginine methyl ester, 5 mg/kg iv). ET augmented the vasoconstrictor response to sympathetic stimulation in a training intensity-dependent manner (P < 0.05) (S: 2 Hz: -26 ± 7.1%; 20 Hz: -26.9 ± 7.3%; 40 Hz: -27.7 ± 7.0%; M: 2 Hz: -37.4 ± 8.3%; 20 Hz: -35.9 ± 7.4%; 40 Hz: -38.2 ± 9.4%; H: 2 Hz: -46.9 ± 7.8%; 20 Hz: -48.5 ± 7.2%; 40 Hz: -51.2 ± 7.3%). O2(-) scavenging did not alter (P > 0.05) the vasoconstrictor response in S rats (S: 2 Hz: -23.9 ± 7.6%; 20 Hz: -26.1 ± 9.1%; 40 Hz: -27.5 ± 7.2%), whereas the response in ET rats was diminished (M: 2 Hz: -26.3 ± 5.1%; 20 Hz: -28.7 ± 5.3%; 40 Hz: -28.5 ± 5.6%; H: 2 Hz: -35.5 ± 10.3%; 20 Hz: -38.6 ± 6.8%; 40 Hz: -43.9 ± 5.9%, P < 0.05). TIRON + N(ω)-nitro-l-arginine methyl ester increased vasoconstrictor responsiveness (P < 0.05) in ET rats (M: 2 Hz: -47.7 ± 9.8%; 20 Hz: -41.2 ± 7.2%; 40 Hz: -50.5 ± 7.9%; H: 2 Hz: -55.8 ± 7.6%; 20 Hz: -55.7 ± 7.8%; 40 Hz: -58.7 ± 6.2%), whereas, in S rats, the response was unchanged (2 Hz: -29.4 ± 8.7%; 20 Hz: -30.0 ± 7.4%; 40 Hz: -35.2 ± 10.3%; P > 0.05). These data indicate that the augmented sympathetic vasoconstrictor responsiveness in ET rats was related to increased oxidative stress and altered nitric oxide-mediated inhibition of vasoconstriction.