title: Vascular responsiveness in alloxan-induced diabetes-susceptible (ALS) and resistant (ALR) mice.
abstract: Changes in reactivity of vascular smooth muscles of male alloxan-induced diabetes-susceptible (ALS) and resistant (ALR) mice aorta were investigated at 2 weeks, 1, 2 and 4 month(s) after the injection of alloxan (45 mg/kg, i.v.). The glucose levels in blood and urine of all the alloxan-treated ALS mice were markedly elevated while those in alloxan-treated ALR and non-treated ALS and ALR mice were not altered. The magnitude of high K+ (65.4 mM)-induced contractions were not affected by the treatment of alloxan. Norepinephrine-induced contractions in vascular smooth muscles of ALS mice in a diabetic state for 2 or 4 months were significantly potentiated. The contractile sensitivity to prostaglandin F2 alpha (PGF2 alpha) was increased in the 4-month-diabetic state. Responsiveness to 5-HT did not vary in the diabetic mouse. Vasorelaxation induced by nitroprusside was attenuated in 2 weeks, 2 or 4 month-diabetic ALS mice. Similarly the inhibitory effects of levcromakalim were attenuated at 2 and 4 months. The influences of diabetes on the inhibitory effects of forskolin or verapamil were very small or not detected. The effects of the vasomodulators used in this study on the vascular smooth muscles of alloxan-treated ALR mice did not differ from those of untreated ALR mice. The results from using ALS and ALR mice suggest that the vasoreactivities to some vasomodulators are changed especially in the long-term diabetic state and that when diabetes was not induced the dose of alloxan does not have any effect on vascular smooth muscle.
authors.affiliation: Department of Animal Science and Technology, Faculty of Agriculture, Okayama University, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Abe
authors.forename: C
authors.initials: C
authors.lastname: Kawazoe
authors.forename: Y
authors.initials: Y
authors.lastname: Kondo
authors.forename: K
authors.initials: K
authors.lastname: Sato
mesh_terms: D000496:Alloxan; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D019806:Cromakalim / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D015237:Dinoprost / Q000494:pharmacology; D004195:Disease Models, Animal; D004198:Disease Susceptibility / Q000662:veterinary; D006029:Glycosuria / Q000378:metabolism; D008297:Male; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D019806:Cromakalim; D009599:Nitroprusside; D000496:Alloxan; D015237:Dinoprost; D011188:Potassium; D009638:Norepinephrine