Abstract
The exercise pressor reflex is amplified in patients with peripheral artery disease (PAD) and in an experimental PAD model of rats induced by femoral artery occlusion. Heightened blood pressure worsens the restricted blood flow directed to the limbs in this disease. The purpose of this study was to determine the role played by muscle oxidative stress in regulating the augmented pressor response to static exercise in PAD. We hypothesized that limb ischemia impairs muscle superoxide dismutase (SOD) thereby leading to abnormal autonomic responsiveness observed in PAD animals, and a chronic compensation of SOD for anti-oxidation improves the exaggerated exercise pressor reflex. Our data show that femoral occlusion decreased the protein levels of SOD in ischemic muscle as compared with control muscle. Downregulation of SOD appeared to a greater degree in the oxidative (red) muscle than in the glycolytic (white) muscle under the condition of muscle ischemia. In addition, the exercise pressor response was assessed during electrically induced static contraction. The data demonstrates that the enhancement of the exercise pressor reflex was significantly attenuated after tempol (a mimetic of SOD, 30 mg over a period of 72 h) was administered into the occluded hindlimb. In the occluded rats, mean arterial pressure (MAP) response was 26 ± 3 mmHg with no tempol and 12 ± 2 mmHg with tempol application (P < 0.05 vs. group with no tempol; n = 6 in each group). There were no differences in muscle tension development (time-tension index: 12.1 ± 1.2 kgs with no tempol and 13.5 ± 1.1 kgs with tempol; P > 0.05 between groups). In conclusion, SOD is lessened in the ischemic muscles and supplement of SOD improves the amplified exercise pressor reflex, which is likely beneficial to the restricted blood flow to the limbs in PAD.
Highlights
During exercise, sympathetic nervous activity (SNA) increases and this leads to rises in blood pressure (BP) and heart rate (HR), myocardial contractility and peripheral vasoconstriction (Victor et al, 1988; Sinoway et al, 1989)
Tiron was not observed to have the inhibitory effects on the exercise pressor reflex in either freely perfused rats or occluded rats when was given in the same way (McCord et al, 2011)
It is noted that in this prior study tempol or tiron was trapped in the muscles and ∼10– 15 min later the hindlimb muscle was reperfused and contracted
Summary
Sympathetic nervous activity (SNA) increases and this leads to rises in blood pressure (BP) and heart rate (HR), myocardial contractility and peripheral vasoconstriction (Victor et al, 1988; Sinoway et al, 1989). This autonomic reflex is initiated as thin fiber afferents arising from contracting skeletal muscle are engaged (McCloskey and Mitchell, 1972; Mitchell et al, 1983; Kaufman and Forster, 1996). Group III afferents are predominantly mechanically sensitive (mechanoreceptor) and Group IV afferents are predominantly metabosensitive (metaboreceptor) (Kaufman et al, 1984). When these receptors are stimulated, thin fiber muscle afferent nerves are engaged, cardiovascular nuclei in the brainstem are activated, SNA increases and BP and HR rise (Mitchell et al, 1983)
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