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Articles in PresS, published online ahead of print September 13, 2002
J Appl Physiol, 10.1152/jap.00246.2002
Submitted on March 25, 2002
Accepted on September 11, 2002
1 Departments of Veterinary Biomedical Sciences, Physiology and Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA; Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA; Physiology, University of Missouri, Columbia, MO, USA
2 Departments of Veterinary Biomedical Sciences, Physiology and Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
3 Department of Kinesiology, University of Waterloo, Waterloo, ON, Canada; Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
4 Departments of Veterinary Biomedical Sciences, Physiology and Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA; Physiology, University of Missouri, Columbia, MO, USA
5 Departments of Veterinary Biomedical Sciences, Physiology and Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA; Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
6 Departments of Veterinary Biomedical Sciences, Physiology and Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA; ; Department of Kinesiology, University of Waterloo, Waterloo, ON, Canada
* To whom correspondence should be addressed. E-mail: laughlinm{at}missouri.edu.
Our objective was to test the hypothesis that short-term exercise training (STR) of pigs increases bradykinin-induced, endothelium-dependent dilation of conduit coronary arteries but not coronary arterioles. Female, Yucatan miniature swine ran on a treadmill for 1 hr, at 3.5 mph, twice daily for 7 days (STR; n=28). Skeletal muscle citrate synthase activity was increased in STR compared with sedentary controls (SED; n=26). Vasoreactivity was evaluated in isolated segments of conduit arteries (1-2 mm I.D., 3-4 mm length) mounted on myographs and in arterioles (50-100 µm I.D.) isolated and cannulated with micropipettes with intraluminal pressure set at 60 cm H2O. Endothelium-dependent relaxation/dilation was assessed by examining responses to increasing concentrations of bradykinin (BK)(Conduit arteries 10-12-10-6M and arterioles 10-13-10-6 M). There were no differences in maximal BK-induced dilation or BK sensitivity of coronary arterioles from SED and STR hearts. In contrast, sensitivity of conduit arteries (precontracted with PGF2
) to BK was increased significantly (p < 0.05) in STR (EC50, 2.33 ± 0.62 nM, n=12) compared to SED (EC50, 3.88 ± 0.62 nM, n=13). The potential role of changes in endothelial nitric oxide synthase (eNOS) and superoxide dismutase (SOD-1) expression in these changes in BK-induced dilation was evaluated with immunoblot analysis. There was no difference in eNOS levels of STR and SED conduit coronary arteries. In contrast, STR exhibited significant increases in eNOS protein in aortic endothelial cells. Neither protein or mRNA levels of eNOS were different in coronary arterioles from STR compared to SED arterioles. STR did not alter expression of SOD-1 in any artery examined. We conclude that pigs exhibit increases in endothelium-dependent responses of conduit arteries and an apparent lack of change in endothelium-dependent responses in coronary arterioles at the onset of exercise training. These adaptations in pigs do not appear to be mediated by alterations in eNOS or SOD-1 expression.
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