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首页> 外文期刊>Life sciences >Nociceptin/orphanin FQ increases ANP secretion in neonatal cardiac myocytes.
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Nociceptin/orphanin FQ increases ANP secretion in neonatal cardiac myocytes.

机译：Nociceptin / orphanin FQ可增加新生儿心肌细胞中ANP的分泌。

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摘要

Nociceptin (N/OFQ) is a novel heptadecapeptide with an amino acid sequence similar to that of endogenous opioid peptide dynorphin A. Dynorphin have been reported to increase the secretion of atrial natriuretic peptide (ANP) via selective activation of kappa-opioid receptor in cultured atrial cardiocytes. The present study was designed to investigate the direct effect of N/OFQ on the ANP secretion in cultured neonatal rat cardiac myocytes via N/OFQ receptor (NOP) activation. The secretion of ANP from cultured neonatal cardiac myocytes was increased in terms of incubation time. N/OFQ, at a dose of 0.3, 1, 3, and 10 microM, caused increases in ANP secretion in a dose-dependent manner. The N/OFQ-induced ANP secretion was completely antagonized by antagonists of NOP, 1 microM each of [Phe1 (CH2-NH) Gly2] nociceptin (1-13)-NH2 ([FG]N/OFQ(1-13)NH2) or naloxone benzoylhydrazone. In contrast, naloxone (1 microM), the non-selective opioid receptor antagonist, did not alter ANP response to N/OFQ. N/OFQ at 3 microM inhibited basal and forskolin-stimulated cAMP production, which was partially antagonized with the pretreatment of [FG]N/OFQ(1-13)NH2. An increase in ANP secretion by N/OFQ was also partially blocked by the pretreatment of forskolin. Homologous competition studies in neonatal cardiomyocyte membranes revealed the presence of two distinct sites. The high affinity site (10.9 +/- 1.6 nM) was far less abundant than the low affinity site. Therefore, these results suggest that N/OFQ causes an increase in ANP secretion in cultured neonatal cardiac myocytes by decreasing cAMP through its binding sites.
机译：Nociceptin（N / OFQ）是一种新颖的七肽，其氨基酸序列与内源性阿片肽强啡肽A相似。据报道，强啡肽可通过选择性激活培养的κ阿片受体来增加心钠素的分泌。心房心肌细胞。本研究旨在研究N / OFQ通过N / OFQ受体（NOP）激活对新生大鼠心肌细胞ANP分泌的直接影响。就培养时间而言，培养的新生儿心肌细胞中ANP的分泌增加。 N / OFQ的剂量分别为0.3、1、3和10 microM，导致ANP分泌呈剂量依赖性。 N / OFQ诱导的ANP分泌被NOP拮抗剂完全拮抗，NOP拮抗剂分别[Phe1（CH2-NH）Gly2] Nociceptin（1-13）-NH2（[FG] N / OFQ（1-13）NH2每个1 microM ）或纳洛酮苯甲酰hydr。相反，非选择性阿片受体拮抗剂纳洛酮（1 microM）不会改变ANP对N / OFQ的反应。 N / OFQ为3 microM会抑制基础和福司柯林刺激的cAMP产生，而[FG] N / OFQ（1-13）NH2的预处理则部分拮抗了cAMP的产生。 N / OFQ对ANP分泌的增加也被毛喉素的预处理部分阻止。新生儿心肌细胞膜上的同源竞争研究表明存在两个不同的位点。高亲和力位点（10.9 +/- 1.6 nM）远不如低亲和力位点丰富。因此，这些结果表明，N / OFQ通过减少通过其结合位点的cAMP导致培养的新生儿心肌细胞中ANP分泌的增加。

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