Zhang Jing, He Chunbo, Pi Xiong, Wang Yan, Zhou Lanxia, Dong Shouliang
Institute of Biochemistry and Molecular Biology, School of Life Sciences, 222 Tianshui South Road, Lanzhou 730000, China.
The Core Laboratory of the First Affiliated Hospital, Lanzhou University, 1 Donggang West Road, Lanzhou 730000, China; Key Laboratory for Gastrointestinal Diseases of Gansu Province, Lanzhou 730000, China.
Eur J Pharmacol. 2016 Dec 5;792:33-37. doi: 10.1016/j.ejphar.2016.10.028. Epub 2016 Oct 23.
The interactions of the chimeric peptide MCRT (YPFPFRTic-NH), based on morphiceptin and neuropeptide FF derivative PFRTic-NH, on the effects of endokinin A/B (EKA/B) on mean arterial blood pressure of the urethane-anaesthetized rat have been investigated in the absence and presence of tachykinin receptor antagonists, naloxone and NO synthase inhibitors. While MCRT produced dose dependent decreases in mean arterial pressure, in its presence only a small but statistically insignificant decreases in the magnitude and the time course of the depressor effect of EKA/B (10nmol/kg) were observed. MCRT had little influence on the depressor effect of EKA/B (1 nmol/kg), but strongly potentiated that of EKA/B (100nmol/kg). The tachykinin NK receptor antagonist SR140333B (1mg/kg) and the NK antagonist SR142891 (2.79mg/kg) both reduced the hypotensive effects of EKA/B and MCRT alone and blocked those of the two peptides in combination. The NK antagonist GR159897 (4mg/kg) partially blocked the depressor effects of EKA/B and MCRT alone. Naloxone (2mg/kg) completely blocked the depressor effect of MCTR, but partially blocked that of EKA/B. The NO synthase inhibitor l-NAME (50mg/kg) partially blocked the depressor effects of EKA/B, MCRT, and EKA/B + MCRT. These results could help to better understand the role of tachykinin receptors, opioid receptors and neuropeptide FF receptors in cardiovascular system.
基于强啡肽原和神经肽FF衍生物PFRTic-NH的嵌合肽MCRT（YPFPFRTic-NH），在存在和不存在速激肽受体拮抗剂、纳洛酮和一氧化氮合酶抑制剂的情况下，对内皮激肽A/B（EKA/B）对乌拉坦麻醉大鼠平均动脉血压的影响进行了研究。虽然MCRT可使平均动脉压呈剂量依赖性降低，但在其存在的情况下，仅观察到EKA/B（10nmol/kg）降压作用的幅度和时间过程有小幅但无统计学意义的降低。MCRT对EKA/B（1nmol/kg）的降压作用影响不大，但强烈增强了EKA/B（100nmol/kg）的降压作用。速激肽NK受体拮抗剂SR140333B（1mg/kg）和NK拮抗剂SR142891（2.79mg/kg）均降低了EKA/B和单独的MCRT的降压作用，并阻断了两种肽联合使用时的降压作用。NK拮抗剂GR159897（4mg/kg）部分阻断了EKA/B和单独的MCRT的降压作用。纳洛酮（2mg/kg）完全阻断了MCTR的降压作用，但部分阻断了EKA/B的降压作用。一氧化氮合酶抑制剂L-NAME（50mg/kg）部分阻断了EKA/B、MCRT以及EKA/B + MCRT的降压作用。这些结果有助于更好地理解速激肽受体、阿片受体和神经肽FF受体在心血管系统中的作用。
