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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Comparison of glycyrrhetinic acid isoforms and carbenoxolone as inhibitors of EDHF-type relaxations mediated via gap junctions.
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Comparison of glycyrrhetinic acid isoforms and carbenoxolone as inhibitors of EDHF-type relaxations mediated via gap junctions.

机译：甘草次酸同工型和羧苄索酮作为通过间隙连接介导的EDHF型松弛抑制剂的比较。

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摘要

The vascular actions of the lipophilic gap junction inhibitors 18alpha-glycyrrhetinic acid (18alpha-GA), 18beta-glycyrrhetinic acid (18beta-GA) and the water-soluble hemisuccinate derivative of 18beta-GA, carbenoxolone, were investigated in preconstricted rings of rabbit superior mesenteric artery. EDHF-type relaxations to acetylcholine (ACh), observed in the presence of 300 microM NG-nitro-L-arginine methyl ester (L-NAME) and 10 microM indomethacin, were attenuated by preincubation with 18alpha-GA (to 100 microM), 18A-GA (to 10 microM) or carbenoxolone (to 300 microM) in a concentration-dependent fashion. By contrast, none of these agents affected responses to sodium nitroprusside, an exogeneous source of NO, and relaxations evoked by ACh in the absence of L-NAME were attenuated by only approximately 20%. 18alpha-GA exerted no direct effect on vessel tone, whereas 18beta-GA and carbenoxolone caused relaxations which were maximal at approximately 1 and approximately 10 mM, respectively. Relaxations to carbenoxolone were attenuated by endothelial denudation and by incubation with L-NAME, whereas those to 18beta-GA were unaffected. In conclusion, all three agents inhibit EDHF-type relaxations evoked by ACh, providing further evidence for the involvement of gap junctions in such responses. Unlike 18alpha-GA, carbenoxolone and 18beta-GA possess intrinsic vasorelaxant activity which in the case of carbenoxolone involves functional enhancement of NO activity in addition to direct effects on vascular smooth muscle.
机译：亲脂性间隙连接抑制剂18alpha-甘草次酸（18alpha-GA），18beta-甘草次酸（18beta-GA）和18beta-GA的水溶性半琥珀酸酯衍生物羧苄索隆的血管作用在兔上缩环中进行了研究肠系膜动脉。在300 microM NG-硝基-L-精氨酸甲酯（L-NAME）和10 microM吲哚美辛存在下观察到的EDHF型对乙酰胆碱（ACh）的松弛通过与18alpha-GA的预孵育（至100 microM）而减弱， 18A-GA（至10 microM）或羧苄索龙（至300 microM）以浓度依赖性方式存在。相比之下，这些试剂均不影响对硝普钠（一种外源性NO）的反应，在没有L-NAME的情况下ACh引起的舒张作用仅减弱约20％。 18alpha-GA对血管张力没有直接影响，而18beta-GA和羧甲基环戊二烯引起的舒张作用最大，分别在大约1和10 mM处最大。内皮剥脱和与L-NAME的孵育减弱了对羧甲基环戊二烯酮的弛豫，而对18beta-GA的弛豫不受影响。总之，所有三种药物均能抑制ACh引起的EDHF型松弛，为间隙连接参与此类反应提供了进一步的证据。与18alpha-GA不同，羧苄酮和18beta-GA具有固有的血管舒张活性，在羧苄酮的情况下，除了直接作用于血管平滑肌外，还涉及功能性NO活性的增强。

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