Fig. 1

Impairment of vascular ring contraction and dilation by high glucose involves RhoA/ROCK signaling. a Concentration-response curves showing the contractile responses of rat small coronary artery vascular rings treated with 4-AP (a voltage-gated K⁺ channel blocker; 0.1–3 mM) under various experimental conditions. Treatment with high glucose (23 mM D-glucose) was associated with attenuation of contraction of rings treated with 4-AP (compared with 5.5 mM D-glucose) that was partially reversed by C3 transferase (a RhoA inhibitor) and Y-27632 (a ROCK inhibitor). b Rat small coronary artery vascular rings treated with high glucose (23 mM D-glucose) showed an impairment of dilation (compared with 5.5 mM D-glucose) in response to 1 μM forskolin (adenylyl cyclase activator); this impairment was partially reversed by C3 transferase and Y-27632. Data are shown as mean ± SD (n = 6). *P < 0.05 vs. NG. ^#P < 0.05 vs. HG. c Concentration-response curves showing the contractile responses of rat small coronary artery vascular rings to 4-AP (a voltage-gated K⁺ channel blocker; 0.1-3 mM) under various experimental conditions. Treatment with peroxynitrite (5 μM peroxynitrite) was associated with attenuation of contraction of rings treated with 4-AP (compared with 5.5 mM D-glucose and 5 μM decomposed peroxynitrite) that was partially reversed by urate, C3 transferase, and Y-27632. d Rat coronary small coronary artery rings treated with ONOO (5 μM peroxynitrite) showed an impairment of dilation (compared with 5.5 mM D-glucose and 5 μM decomposed peroxynitrite) in response to 1 μM forskolin (adenylyl cyclase activator); this impairment was partially reversed by urate, C3 transferase, and Y-27632. Data are shown as mean ± SD (n = 6). *P < 0.05 vs. ONOO