Dept of Pathology, The 2nd Affiliated Hospital, Shantou University Medical College, Shantou, China.
Cardiovascular Research Center, Shantou University Medical College, Shantou, China.
Sci Rep. 2017 Feb 6;7:42167. doi: 10.1038/srep42167.
Prostacyclin, also termed as prostaglandin I (PGI), evokes contraction in vessels with limited expression of the prostacyclin receptor. Although the thromboxane-prostanoid receptor (TP) is proposed to mediate such a response of PGI, other unknown receptor(s) might also be involved. TP knockout (TP) mice were thus designed and used to test the hypothesis. Vessels, which normally show contraction to PGI, were isolated for functional and biochemical analyses. Here, we showed that the contractile response evoked by PGI was indeed only partially abolished in the abdominal aorta of TP mice. Interestingly, further antagonizing the E-type prostaglandin receptor EP3 removed the remaining contractile activity, resulting in relaxation evoked by PGI in such vessels of TP mice. These results suggest that EP3 along with TP contributes to vasoconstrictor responses evoked by PGI, and hence imply a novel mechanism for endothelial cyclooxygenase metabolites (which consist mainly of PGI) in regulating vascular functions.
前列环素，也称为前列腺素 I（PGI），在前列腺素 I 受体表达有限的血管中引起收缩。尽管血栓烷-前列腺素受体（TP）被认为介导了 PGI 的这种反应，但其他未知的受体也可能参与其中。因此，设计并使用 TP 敲除（TP）小鼠来验证这一假设。将通常对 PGI 产生收缩反应的血管分离出来进行功能和生化分析。在这里，我们表明，TP 小鼠腹主动脉中 PGI 引起的收缩反应确实仅部分被阻断。有趣的是，进一步拮抗 E 型前列腺素受体 EP3 消除了剩余的收缩活性，导致 PGI 在 TP 小鼠的这些血管中引起松弛。这些结果表明，EP3 与 TP 共同导致 PGI 引起的血管收缩反应，这意味着内皮环氧化酶代谢物（主要由 PGI 组成）在调节血管功能方面存在一种新的机制。
