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一氧化氮参与降钙素基因相关肽的血管舒张和降压作用。

Involvement of nitric oxide in the vasodilator and depressor effect of calcitonin gene-related peptide.

作者信息

Tan D Y, Zhang L Z, Zhao Y T, Zhao D, Tang J

机构信息

Institute of Cardiovascular Research, Beijing Medical University.

出版信息

Chin Med J (Engl). 1994 Oct;107(10):745-9.

PMID:7835100
Abstract

In present study, we examined the effects of NG-nitro-L-arginine (LNNA), an inhibitor of nitric oxide synthase (NOS), and/or methylene blue (MB), a blocker of guanylate cyclase on the vasodilator response of isolated rat arteries including aorta and mesenteric artery to calcitonin gene-related peptide (CGRP) by in vitro vasoconstriction experiment, and the effect of LNNA on the depressor action of CGRP by in vivo hemodynamic experiment. Furthermore, the effect of CGRP on NOS activity and cyclic guanylate monophosphate (cGMP) content were also examined by NOS activity assay and radioimmunoassay (RIA), respectively. The results showed that LNNA and/or MB significantly decreased, but not abolished, the vasodilator response of isolated rat aorta and mesenteric artery to CGRP. The depressor effect of CGRP on LNNA-induced hypertensive rats (LHR) was obviously weaker than that on spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR) and normotensive rats (NWR). In addition, CGRP (0.5 nmol/kg) increased the NOS activity of rat aorta tissue by 1.3 times (P < 0.05) and resulted in an increase of cGMP content of aorta (1.27 times, P < 0.05) and myocardium (1.38 times, P < 0.05). The results suggested that NO is involved in the action of CGRP.

摘要

在本研究中,我们通过体外血管收缩实验,研究了一氧化氮合酶(NOS)抑制剂NG-硝基-L-精氨酸(LNNA)和/或鸟苷酸环化酶阻滞剂亚甲蓝(MB)对包括主动脉和肠系膜动脉在内的离体大鼠动脉对降钙素基因相关肽(CGRP)的血管舒张反应的影响,以及通过体内血流动力学实验研究了LNNA对CGRP降压作用的影响。此外,还分别通过NOS活性测定和放射免疫测定(RIA)研究了CGRP对NOS活性和环磷酸鸟苷(cGMP)含量的影响。结果表明,LNNA和/或MB显著降低,但并未消除,离体大鼠主动脉和肠系膜动脉对CGRP的血管舒张反应。CGRP对LNNA诱导的高血压大鼠(LHR)的降压作用明显弱于对自发性高血压大鼠(SHR)、肾性高血压大鼠(RHR)和正常血压大鼠(NWR)的降压作用。此外,CGRP(0.5 nmol/kg)使大鼠主动脉组织的NOS活性增加了1.3倍(P<0.05),并导致主动脉(1.27倍,P<0.05)和心肌(1.38倍,P<0.05)的cGMP含量增加。结果表明,NO参与了CGRP的作用。

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