Insulin reversal of diabetes-induced inhibition of vascular contractility in the rat.
Contractures induced by 10(-9)-10(-4) M phenylephrine (PE) or 10-70 mM KCl were observed in aortas isolated from untreated and insulin-treated streptozotocin-diabetic rats. The experiments were conducted at 2-wk intervals for a 12-wk period after the induction of diabetes. Diabetes caused an average decrease of 58 and 60% in the K and PE contractures, respectively. Although the PE contractures in aortas from the insulin-treated diabetic animals (81%) were significantly greater than those in aortas from the untreated diabetic animals (60%), they were significantly less than those in control tissues (100%). Insulin treatment completely reversed the diabetes-induced decrease in the K contracture (102%). It appears that the diabetes-induced decreases in tension may result from an altered sensitivity of the tissues to KCl but not PE. Histological examination of the tissues revealed that the diminished contractions were not due to any detectable change in mural structure. The data indicate that diabetes-induced inhibition of the mechanisms involved in mediating the K contracture are completely reversible by insulin treatment, whereas those mediating the PE contracture are only partially reversible.
D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000503:physiopathology*; D007328:Insulin / Q000494:pharmacology* / Q000627:therapeutic use; D007700:Kinetics; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology*; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D007328:Insulin; D010656:Phenylephrine