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NPR-C受体参与C型利钠肽对胆汁分泌的反应。

NPR-C receptors are involved in C-type natriuretic peptide response on bile secretion.

作者信息

Sabbatini Maria E, Vatta Marcelo S, Vescina Cristina, Gonzales Soledad, Fernandez Belisario, Bianciotti Liliana G

机构信息

Cátedra de Fisiopatologi;a, Facultad de Farmacia y Bioqui;mica, Universidad de Buenos Aires, Juni;n 956, 5 piso (1113), Buenos Aires, Argentina.

出版信息

Regul Pept. 2003 Nov 15;116(1-3):13-20. doi: 10.1016/s0167-0115(03)00168-x.

Abstract

C-type natriuretic peptide (CNP) is a member of the natriuretic peptide family. Previous studies reported the presence of natriuretic peptide receptors and mRNA CNP in the liver. In the present work, we sought to establish the role of CNP in the regulation of bile secretion in the rat and the possible pathways involved.CNP diminished basal as well as bile salt-evoked bile flow and bile acid output in a dose-dependent manner. It also reduced the excretion of sodium, chloride, and potassium but did not modify bile pH or the excretion of phospholipids, total proteins, and glutathione. Neither parasympathetic nor sympathetic blockade abolished CNP inhibitory response on bile secretion. The selective NPR-C agonist, C-ANP-(4-23) amide, diminished bile flow and the co-administration of both peptides did not further decrease it. CNP did not alter mean arterial pressure or portal venous pressure at any given doses.CNP decreased bile acid-dependent flow without affecting bile acid-independent flow. The inhibitory effect of CNP did not involve the participation of the autonomic nervous system or hemodynamic changes. The participation of NPR-C receptors in CNP response is strongly supported by present findings. The present study shows that CNP modulates bile secretion in the rat, suggesting that CNP may be part of the large family of peptides involved in the regulation of gastrointestinal physiology.

摘要

C型利钠肽(CNP)是利钠肽家族的一员。先前的研究报道肝脏中存在利钠肽受体和CNP信使核糖核酸。在本研究中,我们试图确定CNP在大鼠胆汁分泌调节中的作用以及可能涉及的途径。CNP以剂量依赖的方式减少基础胆汁分泌以及胆盐诱发的胆汁流量和胆汁酸输出。它还减少了钠、氯和钾的排泄,但没有改变胆汁pH值或磷脂、总蛋白和谷胱甘肽的排泄。副交感神经或交感神经阻断均未消除CNP对胆汁分泌的抑制反应。选择性NPR-C激动剂C-ANP-(4-23)酰胺减少了胆汁流量,两种肽共同给药并未进一步降低胆汁流量。在任何给定剂量下,CNP均未改变平均动脉压或门静脉压。CNP降低了胆汁酸依赖性流量,而不影响胆汁酸非依赖性流量。CNP的抑制作用不涉及自主神经系统的参与或血流动力学变化。本研究结果有力支持了NPR-C受体参与CNP反应。本研究表明,CNP调节大鼠胆汁分泌,提示CNP可能是参与胃肠生理学调节的一大类肽的一部分。

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