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Am J Physiol Heart Circ Physiol 274: H1895-H1901, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 6, H1895-H1901, June 1998

Treatment with dimethylthiourea prevents impaired dilatation of the basilar artery during diabetes mellitus

William G. Mayhan and Kaushik P. Patel

Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, Nebraska 68198

The goal of this study was to test the hypothesis that the synthesis/release of hydroxyl radical accounts for impaired nitric oxide synthase-dependent dilatation of the basilar artery during diabetes mellitus. We measured the diameter of the basilar artery in vivo in nondiabetic and diabetic rats (streptozotocin, 50-60 mg/kg ip) in response to nitric oxide synthase-dependent agonists (acetylcholine and substance P) and a nitric oxide synthase-independent agonist (nitroglycerin). Reactivity of the basilar artery was measured in untreated nondiabetic and diabetic rats and in nondiabetic and diabetic rats treated with a daily intraperitoneal injection of dimethylthiourea (DMTU; 50 mg/kg). Injection of DMTU was started 48 h after injection of streptozotocin and was continued throughout the diabetic period (3-4 wk). Topical application of acetylcholine (0.1, 1.0, and 10 µM) and substance P (0.1 and 1.0 µM) produced similar dilatation of the basilar artery in untreated and DMTU-treated nondiabetic rats. In untreated diabetic rats, the magnitude of vasodilation produced by acetylcholine and substance P was significantly less than in untreated nondiabetic rats. However, in DMTU-treated diabetic rats, dilatation of the basilar artery in response to acetylcholine and substance P was similar to that observed in nondiabetic rats. Dilatation of the basilar artery in response to nitroglycerin was similar in untreated and DMTU-treated nondiabetic and diabetic rats. These findings suggest that impaired nitric oxide synthase-dependent dilatation of the basilar artery during diabetes mellitus may be related to the synthesis/release of hydroxyl radical.

nitric oxide; rats; acetylcholine; substance P; NG-monomethyl-L-arginine; nitroglycerin; brain; hydroxyl radical; oxygen radicals


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