Ropivacaine-Induced Contraction Is Attenuated by Both Endothelial Nitric Oxide and Voltage-Dependent Potassium Channels in Isolated Rat Aortae
Figure 2
(a) The effect of endothelial denudation and N ω-nitro-L-arginine methyl ester (L-NAME) on ropivacaine concentration-response curves in isolated aortae. Data are shown as the mean ± SD and expressed as a percentage of the maximal contraction induced by isotonic 60 mM KCl (100% = g [], 100% = g [], and 100% = g [] for untreated endothelium-intact aortae, untreated endothelium-denuded aortae, and endothelium-intact aortae treated with M L-NAME, resp.). N indicates the number of rats from which descending thoracic aortic rings were derived. and versus endothelium-intact aortae. versus M ropivacaine and versus M in endothelium-intact aortae. (b) The effect of N ω-propyl-L-arginine hydrochloride and 1400W dihydrochloride on ropivacaine concentration-response curves in endothelium-intact aortae. Data are shown as the mean ± SD and expressed as a percentage of the maximal contraction induced by isotonic 60 mM KCl (100% = g [], 100% = g [], and 100% = g [] for untreated endothelium-intact aortae, endothelium-intact aortae treated with M N ω-propyl-L-arginine hydrochloride, and endothelium-intact aortae treated with M 1400W dihydrochloride, resp.). N indicates the number of rats from which descending thoracic aortic rings were derived.