Naturally occurring hydroxystilbenes have been shown to induce vasorelaxati
on. Here, we studied the mechanism of resveratrol-induced vasorelaxation in
different types of blood vessels, namely mesenteric (resistance) and main
uterine (conductance) arteries, from female guinea-pigs on day 7 and day 15
of the oestrous cycle. Resveratrol (5-70 mu mol/l) induced concentration-d
ependent relaxation of both mesenteric and uterine arteries preconstricted
with either noradrenaline (NA; 10 mu mol/l) or KCl (125 mmol/l). Resveratro
l was 2-fold more potent in inducing relaxation of mesenteric arteries than
of uterine arteries. Its effects on uterine arteries from both day-7 and d
ay- 15 guinea-pigs were similar, irrespective of the constrictor used, but
it was significantly (P < 0.01) more potent in inducing relaxation of mesen
teric arteries contracted with NA compared with those constricted with KCl.
In day-7 arteries precontracted with NA, N-G-nitro-L-arginine methyl ester
(L-NAME; 10 mu mol/l) had no effects on the time course of resveratrol-ind
uced vasorelaxation in either mesenteric or uterine arteries. However, indo
methacin (50 mu mol/l) significantly (P < 0.05) potentiated resveratrol's e
ffect on mesenteric, but nor uterine, arteries. Indomethacin had no effect
on resveratrol-induced vasorelaxation of arteries contracted with KCl, wher
eas L-NAME significantly (P < 0.05) reduced the effects of resveratrol on u
terine, bur not on mesenteric, arteries. In day-15 arteries, L-NAME signifi
cantly (P < 0.01) attenuated the effects of resveratrol on mesenteric arter
ies contracted with NA. Indomethacin had no effect on resveratrol activity.
This study indicates that: (a) the effect of resveratrol on resistance art
eries is greater than that on conductance arteries; (b) the effects of resv
eratrol are not mediated via prostanoids, but NO may play a role; and (c) t
he stage of the oestrous cycle has no influence on resveratrol-induced vaso
relaxation.