Hi. Chen et Ht. Li, PHYSICAL CONDITIONING CAN MODULATE ENDOTHELIUM-DEPENDENT VASORELAXATION IN RABBITS, Arteriosclerosis and thrombosis, 13(6), 1993, pp. 852-856
To investigate whether exercise training can modulate endothelium-depe
ndent 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-degrees grade
for 10-60 minutes/day, 5 days/week for 8 weeks. After exercise traini
ng, the resting heart mte was lowered (p < 0.05). At the end of the ex
periments, three vessel segments, i.e., the thoracic aortas, the pulmo
nary arteries, and the common carotid arteries, were isolated and prec
ontracted with norepinephrine. Acetylcholine-stimulated endothelium-de
rived relaxing factor (EDRF) release was assessed by bioassay in the p
resence Of indomethacin (10(-5) 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 ionop
hore, and to sodium nitroprusside, a direct vasodilator of vascular sm
ooth muscle, were compared between control and trained groups to furth
er investigate possible underlying mechanisms. The results indicated t
hat after exercise training 1) both the thoracic aorta and pulmonary a
rtery, but not the carotid artery, became more sensitive to acetylchol
ine-induced vasorelaxation; 2) no significant differences in basal rel
ease of EDRF between control and trained rabbits were observed; and 3)
there were no significant differences in the vascular responses to A2
3187 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 elevate
d sensitivity to acetylcholine may not be caused by the alteration of
the relaxing response in vascular smooth muscle.