Reactivity to Nitric Oxide in the Caudal Artery from Diabetic Rats

The vascular actions of nitric oxide have been examined in the perfused caudal artery from diabetic rats pretreated with streptozotocin (STZ, 65 mg/kg, i.v.), and age–matched control rats pretreated with vehicle (0.02 M citrate saline, i.v.). In arteries precontracted with phenylephrine, acetylcholine and papaverine produced relaxant responses which were similar for STZ-treated and vehicle-treated rats at 2, 4 and 8 weeks after injection. Relaxant responses to sodium nitroprusside were significantly attenuated in arteries from 2- and 4-week STZ-treated rats, but were significantly enhanced in arteries from 8-week STZ-treated rats compared to the corresponding vehicle-treated rats. In addition, nitric oxide-induced relaxations were significantly greater in arteries from 8-week STZ-treated rats than from vehicle-treated rats. Vasoconstrictor responses to nerve stimulation were not different in arteries from STZ- d vehicle-treated rats 4 and 8 weeks after treatment. The nitric oxide synthase inhibitor, NG -nitro-L-arginine (10 μM), caused a similar degree of enhancement of the vasoconstrictor responses to nerve stimulation in arteries from STZ- and vehicle-treated rats. The results suggest that diabetes caused alterations in reactivity to exogenously added but not endogenously released nitric oxide in the rat caudal artery. Furthermore, nitric oxide-mediated modulation of stimulation-induced vasoconstriction was unaffected by the diabetic state.