Contractile and relaxing activity of arterial smooth muscle from streptozotocin-diabetic rats.
Contractures induced by 10(-4)M phenylephrine (PE) and 70 mM KCl and their relaxation by 10(-2) M theophylline (theo) were observed in aortae isolated from untreated and insulin-treated streptozotocin-diabetic rats for 12 weeks after the induction of diabetes. Diabetes consistently caused an average decrease of 40% in the PE and K-contractures. Treatment of diabetic animals with 2.0-3.5 units (U) of Neutral Protamine Hagedorn (NPH) insulin/day/partially prevented diabetes-induced decreases in the PE contractures while completely preventing them in the K-contractures. Relaxation of the PE-contracture, which was more susceptible to theo than was the K-contracture in control tissues, was not affected by either untreated or insulin-treated diabetes until 12 weeks after the induction of diabetes. While in vivo insulin treatment did not reverse diabetes-induced decreases in the theo-induced relaxation of the PE contracture, it did prevent the diabetes-induced increase in the relaxation of the K-contracture which was observed after 4 weeks. The results indicate that while the mechanisms involved in mediating the PE and K-contractures are inhibited by diabetes, insulin is more effective at preventing the effects of diabetes on the K-contracture and its relaxation than on the induction and relaxation of the PE-contracture.
D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D007328:Insulin / Q000494:pharmacology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D013806:Theophylline / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D001786:Blood Glucose; D007328:Insulin; D010656:Phenylephrine; D013806:Theophylline