Secretin: a hormone for HCO3- homeostasis.

IF 2.9 4区 医学 Q2 PHYSIOLOGY
Peder Berg, Samuel L Svendsen, Niklas Ayasse, Mads Vaarby Sorensen, Jens Leipziger
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Abstract

Secretin is a key hormone of the intestinal phase of digestion which activates pancreatic, bile duct and Brunner gland HCO3- secretion. Recently, the secretin receptor (SCTR) was also found in the basolateral membrane of the beta-intercalated cell (B-IC) of the collecting duct. Experimental addition of secretin triggers a pronounced activation of urinary HCO3- excretion, which is fully dependent on key functional proteins of the B-IC, namely apical pendrin and CFTR and the basolateral SCTR. Recent studies demonstrated that the SCTR knock-out mouse is unable to respond to an acute base load. Here, SCTR KO mice could not rapidly increase urine base excretion, developed prolonged metabolic alkalosis and exhibited marked compensatory hypoventilation. Here, we review the physiological effects of secretin with distinct focus on how secretin activates renal HCO3- excretion. We describe its new function as a hormone for HCO3- homeostasis.

Abstract Image

胰泌素:一种促进 HCO3- 平衡的激素。
胰泌素是肠道消化阶段的一种关键激素,它能激活胰腺、胆管和布鲁纳腺的 HCO3- 分泌。最近,在集合管β间质细胞(B-IC)的基底侧膜上也发现了胰泌素受体(SCTR)。实验性添加分泌素可明显激活尿液中 HCO3- 的排泄,这完全依赖于 B-IC 的关键功能蛋白,即顶端的垂体促肾上腺皮质激素和 CFTR 以及基底侧的 SCTR。最近的研究表明,SCTR基因敲除小鼠无法对急性基础负荷做出反应。在这里,SCTR KO 小鼠不能快速增加尿碱排泄,出现长时间的代谢性碱中毒,并表现出明显的代偿性通气不足。在此,我们回顾了胰泌素的生理效应,并特别关注胰泌素如何激活肾脏 HCO3- 排泄。我们描述了其作为 HCO3- 平衡激素的新功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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