Abstract
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.
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