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首页> 外文期刊>Life sciences >Endothelium-dependent and -independent vasorelaxation induced by CIJ-3-2F, a novel benzyl-furoquinoline with antiarrhythmic action, in rat aorta.
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Endothelium-dependent and -independent vasorelaxation induced by CIJ-3-2F, a novel benzyl-furoquinoline with antiarrhythmic action, in rat aorta.

机译：CIJ-3-2F（一种具有抗心律不齐作用的新型苄基呋喃喹啉）在大鼠主动脉中诱导的内皮依赖性和非依赖性血管舒张。

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AIMS: This study was designed to examine the mechanism of relaxation induced by CIJ-3-2F, a benzyl-furoquinoline antiarrhythmic agent, in rat thoracic aorta at the tissue and cellular levels. MAIN METHODS: Isometric tension of rat aortic ring was measured in response to drugs. Ionic channel activities in freshly dissociated aortic vascular smooth muscle cells (VSMCs) were investigated using a whole-cell patch-clamp technique. KEY FINDINGS: CIJ-3-2F relaxed both phenylephrine (PE) and high KCl (60mM)-induced contractions with respective pEC(50) (-log EC(50)) values of 6.91+/-0.07 and 6.32+/-0.06. Removal of endothelium or pretreatment with nitric oxide (NO)-pathway inhibitors N(omega)-nitro-l-arginine methyl ester (L-NAME), N(G)-monomethyl-l-arginine (L-NMMA), N(5)-(1-iminoethyl)-l-ornithine (L-NIO), hemoglobin, methylene blue or 1H-[1,2,4]oxadiazolo[4,2-alpha]quinoxalin-1-one (ODQ) reduced the relaxant effect of CIJ-3-2F. Relaxation to CIJ-3-2F was also attenuated by K(+) channel blockers tetraethylammonium (TEA) or 4-aminopyridine (4-AP), but not by charybdotoxin plus apamin, iberiotoxin, glibenclamide, or BaCl(2). CIJ-3-2F non-competitively antagonized the contractions induced by PE, Ca(2+), and Bay K8644 in endothelium-denuded rings. In addition, CIJ-3-2F inhibited both the phasic and tonic contractions induced by PE but did not affect the transient contraction induced by caffeine. CIJ-3-2F reduced the Ba(2+) inward current through L-type Ca(2+) channel (IC(50)=4.1microM) and enhanced the voltage-dependent K(+) (K(v)) current in aortic VSMCs. SIGNIFICANCE: These results suggest that CIJ-3-2F induced both endothelium-dependent and -independent vasorelaxation; the former is likely mediated by the NO/cGMP pathway whereas the latter is probably mediated through inhibition of Ca(2+) influx or inositol 1,4,5-triphosphate (IP(3))-sensitive intracellular Ca(2+) release, or through activation of K(v) channels.
机译：目的：本研究旨在检查大鼠胸主动脉CIJ-3-2F（一种苄基-呋喃喹啉抗心律不齐药物）在组织和细胞水平上引起的松弛机制。主要方法：测量药物对大鼠主动脉环的等轴测张力。使用全细胞膜片钳技术研究了新鲜离解的主动脉血管平滑肌细胞（VSMC）中的离子通道活性。主要发现：CIJ-3-2F放松了苯肾上腺素（PE）和高KCl（60mM）诱导的收缩，其pEC（50）（-log EC（50））值分别为6.91 +/- 0.07和6.32 +/- 0.06 。去除内皮或用一氧化氮（NO）通路抑制剂进行预处理N（ω）-硝基-1-精氨酸甲酯（L-NAME），N（G）-单甲基-1-精氨酸（L-NMMA），N（ 5）-（1-亚氨基乙基）-1-鸟氨酸（L-NIO），血红蛋白，亚甲蓝或1H- [1,2,4]恶二唑并[4,2-α]喹喔啉-1-酮（ODQ） CIJ-3-2F的松弛作用。放松到CIJ-3-2F也被K（+）通道阻滞剂四乙铵（TEA）或4-氨基吡啶（4-AP）减弱，但charybdotoxin加上apamin，iberiotoxin，glibenclamide或BaCl（2）却没有。 CIJ-3-2F非竞争性拮抗PE，Ca（2+）和Bay K8644在内皮剥除环中引起的收缩。此外，CIJ-3-2F抑制PE诱导的相变和强直收缩，但不影响咖啡因诱导的瞬时收缩。 CIJ-3-2F减少了通过L型Ca（2+）通道（IC（50）= 4.1microM）的Ba（2+）内向电流并增强了电压依赖性K（+）（K（v））电流在主动脉VSMC中。意义：这些结果表明CIJ-3-2F诱导了内皮依赖性和非依赖性血管舒张。前者可能是由NO / cGMP途径介导的，而后者可能是通过抑制Ca（2+）流入或肌醇1,4,5-三磷酸（IP（3））敏感的细胞内Ca（2+）释放而介导的，或通过激活K（v）渠道。

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