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.