Paraoxon Attenuates Vascular Smooth Muscle Contraction through Inhibiting Ca²⁺ Influx in the Rabbit Thoracic Aorta

Figure 3

Effects of pretreatment with 30𝜇M paraoxon for 30 minutes on Phe- (a) or KCl- (b) induced contraction in endothelium-denuded aortic rings in the presence [Ca²⁺ (+)] or absence [Ca²⁺ (−)] of extracellular Ca²⁺. (c) Percentage of vasodilation induced by 30𝜇M paraoxon or vehicle during Phe- (1 𝜇M) or KCl- (80 mM) induced contraction in endothelium-denuded aortic rings with verapamil pre-treatment for 20 minutes. (d) Effect of pre-treatment with 30𝜇M paraoxon for 30 minutes on Phe- or KCl-induced contraction in endothelium-denuded aortic rings with verapamil (55𝜇M) pre-treatment (20 minutes). (e) Effect of pre-treatment with 30𝜇M paraoxon for 30 minutes on Phe-or KCl-induced contraction in endothelium-denuded aortic rings with ryanodine (30𝜇M) plus nicotinamide (6 mM) pretreatment (20 minutes). (f) Effect of paraoxon on CaCl₂-induced contraction in endothelium-denuded aortic rings prestimulated by 80 mM KCl. Each contractile value was standardized against the contraction level induced by 50 mM KCl in the presence of Ca²⁺ and in the absence of treatment. Data are expressed as means ± SEM (n = 8).^∗𝑃<.05, compared with the vehicle group.

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