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

Figure 1

Paraoxon attenuated phenylephrine- (Phe-) or KCl-induced vasoconstriction in rabbit thoracic aorta. The effect of pretreatment with paraoxon on phenylephrine- (a) or KCl- (b) induced contraction in rabbits thoracic aorta in the presence or absence of aortic endothelium. The aortic ring preparations were preincubated with (30 𝜇M) or without (vehicle) paraoxon for 30 minutes followed by stimulation with Phe (1 𝜇M) or KCl (80 mM). In some ring preparations with aortic endothelium (Endo), L-NNA (30 𝜇M) was incubated during Phe-induced contraction. In some other ring preparations without aortic endothelium, sodium nitroprusside (SNP: 1 nM) and atropine (5𝜇M) were incubated during Phe-induced contraction in the absence of paraoxon. (c) Concentration-response curves for Phe-induced vasoconstriction of endothelium-denuded aortic rings in the presence (0.3𝜇M–30𝜇M) or absence (vehicle) of pretreatment with paraoxon (30𝜇M) for 30 minutes. (d) Concentration-response curves for KCl-induced vasoconstriction of endothelium-denuded aortic rings in the presence (0.3𝜇M–30𝜇M) or absence (vehicle) of paraoxon (pre-treatment for 30 min). Each contractile value was standardized against the contraction level induced by 50 mM KCl in the absence of pretreatment. Data are expressed as means ± SEM (n = 8). ^∗𝑃<.05; ^∗𝑃<.05 compared with the vehicle group.

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