Pimaric acid通过激活BKCa通道和抑制VDCC降低大鼠肺动脉平滑肌的血管收缩

IF 3 3区 医学 Q2 PHARMACOLOGY & PHARMACY
Masashi Ishida , Aya Yamamura , Moe Fujiwara , Taiki Amano , Mina Ota , Yukari Hikawa , Rubii Kondo , Yoshiaki Suzuki , Yuji Imaizumi , Hisao Yamamura
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引用次数: 0

摘要

肺血管在氧气循环中起着关键作用。我们先前证明,PiMA激活了大电导Ca2+激活的K+(BKCa)通道,并抑制了电压依赖性Ca2+通道(VDCC)。在本研究中,PiMA减轻了高K+或内皮素-1诱导的大鼠肺动脉平滑肌(PASMs)的血管收缩。PiMA还降低了高K+诱导的PASM细胞胞浆[Ca2+]的增加。PiMA增加了BKCa电流,降低了VDCC电流。BKCa通道和VDCC分别由α/β1和α1C/α1D/β2/β3亚基形成。这些结果表明,PiMA通过激活PASMs中BKCa通道和抑制VDCC的双重作用诱导血管舒张。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pimaric acid reduces vasoconstriction via BKCa channel activation and VDCC inhibition in rat pulmonary arterial smooth muscles

Pulmonary vessels play a pivotal role in oxygen circulation. We previously demonstrated that pimaric acid (PiMA) activated large-conductance Ca2+-activated K+ (BKCa) channels and inhibited voltage-dependent Ca2+ channels (VDCCs). In the present study, PiMA attenuated vasoconstriction induced by high K+ or endothelin-1 in rat pulmonary arterial smooth muscles (PASMs). PiMA also reduced high K+-induced cytosolic [Ca2+] increase in PASM cells. PiMA increased BKCa currents and decreased VDCC currents. BKCa channels and VDCCs were formed by the α/β1 and α1C1D23 subunits, respectively. These results indicate that PiMA induces vasorelaxation through the dual effects of BKCa channel activation and VDCC inhibition in PASMs.

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来源期刊
CiteScore
6.20
自引率
2.90%
发文量
104
审稿时长
31 days
期刊介绍: Journal of Pharmacological Sciences (JPS) is an international open access journal intended for the advancement of pharmacological sciences in the world. The Journal welcomes submissions in all fields of experimental and clinical pharmacology, including neuroscience, and biochemical, cellular, and molecular pharmacology for publication as Reviews, Full Papers or Short Communications. Short Communications are short research article intended to provide novel and exciting pharmacological findings. Manuscripts concerning descriptive case reports, pharmacokinetic and pharmacodynamic studies without pharmacological mechanism and dose-response determinations are not acceptable and will be rejected without peer review. The ethnopharmacological studies are also out of the scope of this journal. Furthermore, JPS does not publish work on the actions of biological extracts unknown chemical composition.
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