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首页> 外文期刊>Peptides: An International Journal >Effects of urocortin II on neonatal rat cardiac myocytes and non-myocytes.
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Effects of urocortin II on neonatal rat cardiac myocytes and non-myocytes.

机译:urocortin II对新生大鼠心脏肌细胞和非肌细胞的影响。

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摘要

Urocortin (Ucn) II and III, homologous peptides of Ucn that are specific ligands for corticotropin-releasing hormone (CRH) type 2 receptor (CRH-R2), have recently been identified. The present study was designed to elucidate the effects of Ucn II, which is predominantly expressed in rodent heart, on neonatal rat cardiac myocytes (MCs) and cardiac non-myocytes (NMCs). Ucn II increased the incorporation of [3H]-leucine into MCs, as well as the accumulation of cAMP and the secretion of atrial natriuretic peptide. However, no significant changes were demonstrated in NMCs or an MC/NMC co-culture system. The effects of Ucn II were attenuated by astressin2-B, a specific antagonist of CRH-R2, and/or H89, an inhibitor of protein kinase A (PKA). These results indicate that Ucn II may be another endogenous cardiovascular substance that acts via CRH-R2 and the cAMP-dependent PKA pathway.
机译:Urocortin(Ucn)II和III是Ucn的同源肽,它们是促肾上腺皮质激素释放激素(CRH)2型受体(CRH-R2)的特异性配体。本研究旨在阐明主要在啮齿动物心脏中表达的Ucn II对新生大鼠心脏心肌细胞(MCs)和心脏非心肌细胞(NMCs)的影响。 Ucn II增加了[3H]-亮氨酸掺入MC的过程,以及cAMP的积累和心钠素的分泌。但是,在NMC或MC / NMC共培养系统中未发现明显变化。 Ucn II的作用被CRH-R2的特异性拮抗剂astressin2-B和/或蛋白激酶A(PKA)的抑制剂H89减弱。这些结果表明,Ucn II可能是另一种通过CRH-R2和依赖cAMP的PKA途径起作用的内源性心血管物质。

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