Physical conditioning can modulate endothelium-dependent vasorelaxation in rabbits

H I Chen, H T Li
1993 Arteriosclerosis and Thrombosis A Journal of Vascular Biology  
To investigate whether exercise training can modulate endothelium-dependent vasorelaxation, male New Zealand White rabbits were divided into either control or training groups. The training animals were trained on a treadmill with a running speed of 0.88 km/hr on a 0° grade for 10-60 minutes/day, 5 days/week for 8 weeks. After exercise training, the resting heart rate was lowered (p<0.05). At the end of the experiments, three vessel segments, i.e., the thoracic aortas, the pulmonary arteries,
more » ... the common carotid arteries, were isolated and precontracted with norepinephrine. Acetylcholine-stimulated endothelium-derived relaxing factor (EDRF) release was assessed by bioassay in the presence of indomethadn (10~s M). Basal release of EDRF was examined by the addition of hemoglobin. In addition, the relaxing responses of the thoracic aortas and pulmonary arteries to A23187, a calcium ionophore, and to sodium nitroprusside, a direct vasodilator of vascular smooth muscle, were compared between control and trained groups to further investigate possible underlying mechanisms. The results indicated that after exercise training 1) both the thoracic aorta and pulmonary artery, but not the carotid artery, became more sensitive to acetylcholine-induced vasorelaxation; 2) no significant differences in basal release of EDRF between control and trained rabbits were observed; and 3) there were no significant differences in the vascular responses to A23187 or sodium nitroprusside between the two groups. Our data suggest that exercise training may enhance endothelium-dependent vasodilation to acetylcholine via the stimulated EDRF release and that this elevated sensitivity to acetylcholine may not be caused by the alteration of the relaxing response in vascular smooth muscle. (Arteriosclerosis and Thrombosis 1993;13:852-856) KEY WORDS • endurance exercise • endothelium • acetylcholine • rabbits • endotheliumderived relaxing factor T he vascular endothelium is the layer of squamous epithelial cells that is in direct contact with the blood. It not only serves as a diffusion barrier but also displays a variety of biological functions. In 1980, Furchgott and Zawadzki 1 discovered that the response of vascular strips to acetylcholine (ACh) was strongly dependent on the presence of the endothelial cell layer. Their experiments suggested the existence of a mediator passing from endothelial cells to induce the relaxation of vascular smooth muscle. This mediator has been termed endothelium-derived relaxing factor (EDRF). Since then, it was noticed that endothelial cells exert a significant role in the modulation of local vascular tone by the release of endothelium-derived constricting factor and EDRF. 2 -3 Under pathophysiological conditions, the net balance between dilatory and constricting signals is disturbed. Previous studies have indicated that endothelium-dependent relaxation is significantly impaired in atherosclerosis and hypertension, and they suggested that decreased EDRF release may be the principal underlying mechanism re-
doi:10.1161/01.atv.13.6.852 fatcat:voipnqi5vfe2pj4bogxkhfxnxu