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生长抑素对大鼠肠道钙转运的影响。

Effects of somatostatin on intestinal calcium transport in the rat.

作者信息

Favus M J, Berelowitz M, Coe F L

出版信息

Am J Physiol. 1981 Sep;241(3):G215-21. doi: 10.1152/ajpgi.1981.241.3.G215.

Abstract

The addition of somatostatin (SRIF) to rat descending colon in vitro increased the calcium secretory flux from serosa to mucosa (Js leads to m) and reduced tissue short-circuit current (Isc) but did not alter the absorptive flux from mucosa to serosa (Js leads to m). Js leads to m increased by 37% at 10(-9) M SRIF and by 48% at 10(-6) M. The response to SRIF was not altered by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], and SRIF did not interfere with stimulation of calcium Jm leads to s by 1,25(OH)2D3. Removal of sodium from the buffer abolished the stimulation of Js leads to m by SRIF without reducing basal Js leads to m. Secretory fluxes of mannitol and calcium were strongly correlated in the presence and absence of SRIF, suggesting that SRIF stimulates a paracellular transepithelial pathway for calcium. In the duodenum, SRIF altered neither calcium Js leads to m nor Isc. In the ileum, calcium Js leads to m increased and Isc decreased, as in the colon, but only by 28 and 12%, respectively. The maximal change in calcium Js leads to m caused by SRIF in these three intestinal segments was negatively correlated with the tissue concentration of immunoreactive SRIF. These results suggest that intestinal calcium secretion could, in part, be regulated by intestinal SRIF.

摘要

在体外向大鼠降结肠添加生长抑素(SRIF)可增加从浆膜到黏膜的钙分泌通量(Js导致m),并降低组织短路电流(Isc),但不会改变从黏膜到浆膜的吸收通量(Js导致m)。在10^(-9) M SRIF时,Js导致m增加37%,在10^(-6) M时增加48%。1,25 - 二羟维生素D3 [1,25(OH)2D3] 不会改变对SRIF的反应,且SRIF不会干扰1,25(OH)2D3对钙Jm导致s的刺激。从缓冲液中去除钠可消除SRIF对Js导致m的刺激,而不会降低基础Js导致m。在有和没有SRIF的情况下,甘露醇和钙的分泌通量密切相关,表明SRIF刺激了钙的细胞旁跨上皮途径。在十二指肠中,SRIF既不改变钙Js导致m也不改变Isc。在回肠中,钙Js导致m增加,Isc降低,与结肠情况相同,但分别仅增加28%和降低12%。在这三个肠段中,SRIF引起的钙Js导致m的最大变化与免疫反应性SRIF的组织浓度呈负相关。这些结果表明,肠道钙分泌可能部分受肠道SRIF调节。

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