Functional dilatory response in streptozotocin-induced diabetic rats was in
vestigated using thoracic aortas, isolated hearts, and mesenteric beds. Dos
e-response curves to the PGI(2) analogue iloprost on phenylephrine-preconst
ricted rings of diabetic rats and controls were comparable. In contrast, de
creased vasodilation in diabetic rats was observed when dose-response curve
s to iloprost were performed in hearts and on phenylephrine-preconstricted
mesenteric beds. Dose-response curves to forskolin, an adenylyl cyclase act
ivator, performed with hearts and phenylephrine-preconstricted aortic rings
and isolated mesenteric beds of diabetic rats and controls were comparable
. However, a decreased vasodilation to the ATP-sensitive potassium channel
(K-ATP) activator lemakalim was observed in diabetic hearts, but not in aor
tic rings and mesenteric beds. In conclusion, under our experimental condit
ions, diabetes mellitus affects the vasodilation to iloprost in both corona
ry and mesenteric beds, but not in the aorta. In the heart, this modificati
on of vascular reactivity may be due to a decrease in K-ATP channel mediate
d response and not to a decreased activity of adenylyl cyclase. At this tim
e, in the isolated mesenteric bed, the mechanism of this modification in va
scular reactivity remains unknown.