Modification of vasodilator response in streptozotocin-induced diabetic rat

Citation
Jf. Bouchard et al., Modification of vasodilator response in streptozotocin-induced diabetic rat, CAN J PHYSL, 77(12), 1999, pp. 980-985
Citations number
28
Categorie Soggetti
Pharmacology & Toxicology
Journal title
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
ISSN journal
00084212 → ACNP
Volume
77
Issue
12
Year of publication
1999
Pages
980 - 985
Database
ISI
SICI code
0008-4212(199912)77:12<980:MOVRIS>2.0.ZU;2-K
Abstract
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.