We examined the endothelium-dependent relaxation response to acetylcholine
(Ach) in streptozotocin-induced diabetic rat aorta at the stages of 2- and
6-wks' duration in vitro, and compared with another two groups which were t
reated with dietary supplement of 0.1% Aminoquanidine (AG) and 0.5% Erigero
n breviscapus(EB) from 1-week of diabetes induction. At the stage of 2-wks'
duration of diabetes, relaxation responses to lower concentrations of Ach
in 0.3uM phenylepherine-precontracted aortas were diminished significantly
(P<0.05) compared with age-matched control, but the maximal relaxation of A
ch remained unchanged. At the stage of 6-wks' duration, diabetes caused an
approximately 60% (P<0.001) deficit in maximum relaxation, and this was sig
nificantly (P<0.001) prevented in AG and EB treated groups. There was an ap
proximately 40% enhancement in the maximum contractile response to phenylep
herine with diabetes (P<0.05), which was unaffected significantly by AG and
EB treatments. The data suggest that the defective endothelium-dependent r
elaxation in diabetic rat aorta occurred as early as 2-wks' duration of dia
betes, and the treatments of AG and EB could protect vascular endothelium a
lthough the deficits in vascular smooth muscle contractile responses were n
ot protected.