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Am J Physiol Heart Circ Physiol 279: H520-H527, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 2, H520-H527, August 2000

Depressed modulation of oxygen consumption by endogenous nitric oxide in cardiac muscle from diabetic dogs

Gong Zhao, Xiaoping Zhang, Xiaobin Xu, Michael S. Wolin, and Thomas H. Hintze

Department of Physiology, New York Medical College, Valhalla, New York 10595

Our previous study indicated that nitric oxide (NO)-dependent coronary vasodilation was impaired in conscious dogs with diabetes. Our goal was to determine whether modulation of O2 consumption by NO is depressed in canine cardiac muscle after diabetes. Diabetes was induced by injection of alloxan (40-60 mg/kg iv), dogs were killed after diabetes was induced (4-5 wk), and the cardiac muscle from the left ventricle was cut into 15- to 30-mg slices. O2 uptake by the muscle slices was measured polarographically with a Clark-type O2 electrode. S-nitroso-N-acetylpenicillamine decreased O2 consumption in normal and diabetic tissues (10-4 M, 61 ± 7 vs. 61 ± 8%, P > 0.05). Bradykinin (10-4 M)- or carbachol (CCh, 10-4 M)-induced inhibition of O2 consumption was impaired in diabetic tissues (51 ± 6 vs. 17 ± 4% or 48 ± 4 vs. 19 ± 3%, respectively, both P < 0.05 compared with normal). The inhibition of O2 consumption by kininogen or kallikrein was depressed in diabetic tissues as well. In coronary microvessels from diabetic dogs, bradykinin or ACh (10-5 M) caused smaller increases in NO production than those from normal dogs. Our results indicate that the modulation of O2 consumption by endogenous, but not exogenous, NO is depressed in cardiac muscle from diabetic dogs, most likely because of decreased release of NO from the vascular endothelium.

diabetes; kinin


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