Differential modulation of bradykinin-induced relaxation of endothelin-1 and phenylephrine contractions of rat aorta by antioxidants.
Differential modulation of bradykinin-induced relaxation of endothelin-1 and phenylephrine contractions of rat aorta by antioxidants.
复制标题
抗氧化剂对缓激肽诱导的内皮素-1 和去氧肾上腺素舒张大鼠主动脉收缩的差异调节。
DOI：
10.1111/j.1745-7254.2007.00631.x
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发表时间：
2007
影响因子：
8.2
通讯作者：
Yakubu,MomohA
中科院分区：
文献类型：
--
作者：
Anozie,Ogechukwu;Ross,Richonda;Oyekan,AdebayoO;Yakubu,MomohA
Aim:We tested the hypothesis that bradykinin (BK)-induced relaxation of phe-nylephrine (PE) and endothelin-1 (ET-1) contractions can be differentially modulated by reactive oxygen species (ROS).Methods:Aortic rings isolated from Sprague-Dawley rats were used for the study. The contribution of ROS to PE (1× 10− 9− 1× 10− 5 mol/L)-and ET-1 (1× 10− 10− 1× 10− 8 mol/L)-induced contractions and the influence of ROS in BK (1× 10− 9− 1× 10− 5 mol/L) relaxation of PE (1× 10− 7 mol/L) or ET-1 (1× 10− 9 mol/L)-induced tension was evaluated in the aorta in the presence or absence of the following antioxidants: catalase (CAT, 300 U/mL), superoxide dismutase (SOD, 300 U/mL), and vitamin C (1× 10− 4 mol/L).Results:Tension generated by ET-1 (1× 10− 9 mol/L) or PE (1× 10− 7 mol/L) was differentially relaxed by BK (1× 10− 5 mol/L), producing a maximal relaxation of 75%±5% and 35±4%, respectively. The BK (1× 10− 5 mol/L)-induced relaxation of PE (1× 10− 7 mol/L) tension was significantly enhanced from 35%±4%(control) to 56%±9%, 60%±5%, and 49%±6% by SOD, CAT, and vitamin C, respectively (P< 0.05, n= 8). However, the relaxation of ET-1 (1× 10− 9 mol/L) tension was significantly attenuated from 75%±5%(control) to 37%±9%, 63%±4%, and 39%±7% by SOD, CAT, and vitamin C, respectively (P< 0.05, n= 8). On the other hand, CAT had no effect on PE-induced tension, while SOD enhanced PE-induced tension (36%, P< 0.05, n= 10) and vitamin C attenuated (66%, P< 0.05, n= 8) the tension induced by PE. By contrast, SOD or vitamin C had no effect, but CAT attenuated (44%, P< 0.05, n= 9) the tension induced by ET-1.Conclusion:We have demonstrated that O 2− and H 2 O 2 differentially modulate BK relaxation in an agonist-specific manner. O 2− attenuates BK-induced relaxation of PE contraction, but contributes to the relaxation of ET-1 contraction. O 2− seems to inhibit PE contraction, while H 2 O 2 contributes to ET-1-induced contraction. Thus, ROS differentially modulate vascular tone depending on the vasoactive agent that is used to generate the tone.
