Fig. 4.
Overexpression of OGA increased capillary density in the left ventricle (LV) myocardium and restored endothelium-derived hyperpolarization (EDH)-induced relaxation in the coronary arteries in Tie2-Tet-OGA diabetic mice. A: representative capillary images in the LV of control, Dox-treated diabetic, or untreated diabetic heart. Scale bar = 10 μm. B: capillary density [number of capillaries per mm2 (NA/mm2)] in hearts from control, untreated diabetic, and Dox-treated diabetic mice. Values are means ± SE; n = 3 control, 3 untreated diabetic, and 7 Dox-treated diabetic mice. *P < 0.05 vs. control; #P < 0.05 vs. diabetic −Dox. C: endothelium-dependent relaxation by ACh. Coronary artery rings were contracted by treatment with PGF2α, and ACh was administered in a dose-dependent manner. Values are means ± SE; n = 4 per group. *P < 0.05 vs. control; #P <0.05 vs. diabetic −Dox. D: EDH-dependent relaxation induced by ACh in the presence of nitro-l-arginine methyl ester (l-NAME, an eNOS inhibitor, 100 μmol/l) and indomethacin (a cyclooxygenase inhibitor, 10 μmol/l). Values are means ± SE; n = 4 per group. *P < 0.05 vs. control. #P < 0.05 vs. diabetic −Dox. E: sodium nitruprusside (SNP)-induced relaxation (EC-independent). Values are means ± SE; n = 4 per group.