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首页> 外文期刊>Journal of cardiac surgery. >Endothelium-dependent and -independent coronary relaxation induced by urocortin.
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Endothelium-dependent and -independent coronary relaxation induced by urocortin.

机译：urocortin诱导的内皮依赖性和非依赖性冠状动脉舒张。

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摘要

Urocortin, a newly identified polypeptide, possesses cardiac effects. However, the underlying mechanism of its coronary action is still unclear. In the present study we investigated the possible role of endothelial nitric oxide and Ba2+-sensitive K+ channels in the endothelium-dependent relaxant response to urocortin in the isolated rat left anterior descending coronary arteries. Changes of vessel tone were measured in microvessel myographs. Urocortin produced both endothelium-dependent and -independent relaxation with IC50 of 2.52 nM and 16.5 nM, respectively. Denuation of endothelium decreased the relaxing potency of urocortin. In the endothelium-intact rings pretreated with 100 microM N(G)-nitro-L-arginine methyl ester (L-NAME) or 10 microM 1H-[1,2,4]oxadiazolo[4,2-alpha]quinoxalin-1-one (ODQ), the urocortin-induced relaxation was similar to that observed in endothelium-denuded rings. The relaxant response to urocortin was markedly reduced in endothelium-intact rings preconstricted by 35 mM K+. Pretreatment with 100 microM BaCl2 significantly reduced urocortin-induced relaxation without an effect on the maximum relaxation. Combined treatment with BaCl2 plus L-NAME did not produce additive inhibition. In contrast, BaCl2 did not alter urocortin-induced relaxation in the endothelium-denuded rings. In the endothelium-denuded rings, BaCl2 at 100 microM also inhibited nitric oxide donor-induced relaxation. In conclusion, our results suggest that urocortin-induced endothelium-dependent relaxation of rat coronary arteries is primarily mediated by endothelial nitric oxide and subsequent activation of Ba2+-sensitive K+ channels. The urocortin-induced endothelium-dependent relaxation appears to be cyclic GMP-dependent.
机译：新鉴定的多肽乌罗考丁具有心脏效应。然而，其冠脉作用的潜在机制仍不清楚。在本研究中，我们研究了内皮一氧化氮和Ba2 +敏感K +通道在离体大鼠左前降支冠状动脉对尿皮质素的内皮依赖性松弛反应中的可能作用。在微血管肌电图仪中测量血管张力的变化。 Urocortin产生内皮依赖性和非依赖性松弛，IC50分别为2.52 nM和16.5 nM。内皮的变性降低了尿皮质素的松弛能力。在用100 microM N（G）-硝基-L-精氨酸甲酯（L-NAME）或10 microM 1H- [1,2,4]恶二唑并[4,2-α]喹喔啉-1预处理的内皮完整环中-OD（ODQ）时，尿皮质素诱导的松弛类似于在内皮剥脱的环中观察到的松弛。在35mM K +预紧的内皮完整环中，对尿皮质素的松弛反应显着降低。用100 microM BaCl2预处理可显着降低尿皮质素诱导的弛豫，而不影响最大弛豫。 BaCl2加L-NAME的联合处理不会产生加性抑制作用。相比之下，BaCl2不会改变尿皮质素诱导的内皮剥脱环中的松弛。在内皮剥脱的环中，浓度为100 microM的BaCl2也抑制一氧化氮供体引起的松弛。总之，我们的结果表明，尿皮质素诱导的大鼠冠状动脉内皮依赖性舒张主要是由内皮一氧化氮和随后的Ba2 +敏感K +通道激活引起的。尿皮质素诱导的内皮依赖性舒张似乎是循环的GMP依赖性。

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