Lovastatin Incubation Improves Acetylcholine-Induced Relaxation in Isolated Aortic Rings of Diabetic Rat

To evaluate the acute effect of lovastatin on diabetic endothelial dysfunction, we examinedthis effect on the aortic rings of streptozotocin-diabetic rats. the endothelial function wasassessed in aortic rings isolated from diabetic rats, 12 weeks after treatment with streptozotocin(45 mg/kg, i.p.). the concentration-response curve to acetylcholine (ach) in the aortic ringsprecontracted with phenylephrine (10 -6 m) was significantly diminished in diabetic groups; andmaximum relaxation in control and diabetic groups were 82(plus-minus)1.93% and 48(plus-minus)2.39% respectively(a 42% decrease, p(less than)o.ooi). incubation with lovastatin (10-sm) for 10 min, significantlyimproved the ach-induced relaxation of diabetic groups and the maximum relaxation increasedto 74.2 (plus-minus)3.3% (a 54% increase, p(less than)o.ooi).incubation with no -nitro-l-arginine methyl ester hydrochloride (l-name; 5xlo -7 m) for20 min eliminated a significant difference in ach - induced relaxation responses in diabetic andcontrol groups and also eliminated the improving effect of lovastatin in diabetic groups. onthe other hand 10 min incubation with indomethacin (10-s m) did not eliminate the differencein ach-induced relaxation responses in diabetic and control groups and also did not eliminatethe improving effect of lovastatin in diabetic groups. lovastatin did not modify sodiumnitroprosside-induced relaxation in either diabetic or control groups and also did not induce anydirect relaxation.therefore, it is concluded that incubation of aortic rings with lovastatin significantlyimproves endothelium-dependent relaxation in diabetic groups by increasing the nitric oxidebioavailability, most probably due to its' antioxidant effects.