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. 2011 Jul 26;301(5):E882–E888. doi: 10.1152/ajpendo.00037.2011

Fig. 3.

Fig. 3.

GPER-mediated coronary artery relaxation is nitric oxide independent and involves large-conductance, calcium-activated potassium (BKCa) channel activity. A: pretreating (30 min) coronary arteries with 100 μM Nω-nitro-l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase had no effect on G-1-induced relaxation. Each bar represents the mean ± SE (n = 6) B: pretreating vessels (30 min) with 100 nM iberiotoxin (IBTx; 30 min; n = 5) attenuated 1 μM G-1-induced relaxation significantly (*P = 0.001). C: complete concentration-response relationship for G-1-induced relaxation in the absence (■) or presence (○) of 100 nM IBTx (n = 5). *P < 0.05 or lower. Con, control.