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J Appl Physiol (January 29, 2004). doi:10.1152/japplphysiol.01252.2003
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Submitted on November 21, 2003
Accepted on January 26, 2004

EXERCISE TRAINING IMPROVES AORTIC ENDOTHELIUM-DEPENDENT VASORELAXATION AND DETERMINANTS OF NITRIC OXIDE BIOAVAILABILITY IN SPONTANEOUSLY HYPERTENSIVE RATS

Drew A Graham1 and James W Rush1*

1 Department of Kinesiology, University of Waterloo, Waterloo, ON, Canada

* To whom correspondence should be addressed. E-mail: jwerush{at}uwaterloo.ca.

The present study examined in vitro vasomotor function and expression of enzymes controlling nitric oxide (NO) bioavailability in thoracic aorta of adult male normotensive Wistar-Kyoto (WKY) and Spontaneously Hypertensive rats (SHR) that either remained sedentary (SED) or performed six weeks of moderate aerobic exercise training (EX). Training efficacy was confirmed by elevated maximal activities of both citrate synthase (P=0.0024) and {beta}-hydroxyacyl-CoA dehydrogenase (P=0.0073) in the white gastrocnemius skeletal muscle of EX versus SED. Systolic blood pressure was elevated in SHR versus WKY (P<0.0001) but was not affected by exercise training. Despite enhanced sub-maximal endothelium-dependent relaxation to ACh in SHR versus WKY (P=0.0061), maximal endothelium-dependent relaxation was blunted in SED SHR (48±12%) versus SED WKY (84±6%, P=0.0067). Maximal endothelium-dependent relaxation to 10-4 mol/L ACh was completely restored in EX SHR (93±9%) versus SED SHR (P=0.0011). N{omega}-nitro-L-arginine abolished endothelium-dependent relaxation in all groups (P<=0.0001) and caused equal vasocontraction to maximal ACh in SED SHR and EX SHR. Endothelium-independent relaxation to sodium nitroprusside was similar in all groups. Protein levels of endothelial NO synthase (eNOS) were higher in SHR versus WKY (P=0.0157) and in EX versus SED (P=0.0536). Protein levels of the pro-oxidant NAD(P)H oxidoreductase sub-unit, gp91phox, were higher in SHR versus WKY (P<0.0001) and were diminished in EX versus SED (P=0.0557). Levels of the anti-oxidant SOD-1, -2, and catalase enzymes were lower in SHR versus WKY (all P<=0.0005), but were not altered by exercise training. Thus, elevated gp91phox-dependent oxidative stress and reduced anti-oxidant capacity likely contributed to impaired endothelium-dependent vasorelaxation in SED SHR. Furthermore, reduced gp91phox-dependent oxidative stress and enhanced eNOS-derived NO likely contributed to restored endothelium-dependent vasorelaxation in EX SHR.




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