Vascular Effect Of Di-n-butyl Phthalate And The Underlying Mechanism

Aim:To investigate the effect of di-n-butyl phthalate (DBP) on rat arteries and discuss the contraction of vascular rings after incubation with DBP and the influencing mechanism of Vitamin C on these incubated vascular rings. Methods:The perfusion model of the isolated Sprague-Dawley rat thoracic aorta rings was adopted to observe the basal tension in the vasodilatation of DBP(10-6-10-3M) on the isolated rat thoracic aorta rings. To study the contractive reaction of vascular rings after incubation with DBP for30min to KC1and phenylephrine and the same with Vitamin C and DBP for30min. Results:The DBP can contract the thoracic aorta rings with their endothelium preserved or removed in a concentration-dependent manner. The vasoconstriction of endothelium-free (-E) aorta rings was more obvious than that with intact endothelium (+E). In Ca2+free K-H solution, the contraction amplitude of endothelium-free (-E) aorta rings induced by DBP was apparently smaller than that in normal K-H perfusion solution, but showed no significant differences in the control group. Pretreated with verapamil, the aorta rings showed smaller contraction amplitude induced by DBP than that of the single DBP group. Pretreated with Nitric oxide synthase inhibitor (N’-nitro-L-arginine methyl ester hydrochloride, L-NAME), the contraction amplitude was increased in intact endothelium(+E) aorta rings induced by DBP, when pretreated with indomethacin, it had no effect if compared with that of the DBP group. The contraction amplitude of aorta rings after incubation with DBP induced by KC1or PE was lower than that of the control group. There’s no contractive reaction of aorta rings after incubation with Vitamin C. In addition, the contraction amplitude of aorta rings after incubation with DBP and Vitamin C induced by KCl or PE was obviously higher than that after incubation with the only DBP. Conclusion:DBP has vasoconstricting effect in rat arteries. The underlying mechanism of the DBP action may be related to the voltage dependent calcium channels, receptor operated calcium channels and calcium influx. Nitric oxide may participate in the reaction of DBP. The contraction of blood vessel weakened when it’s incubated by DBP. The result may be due to oxidative-stress damage in vascular smooth muscle cells.