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豚鼠回肠肠上皮细胞中H⁺偶联寡肽吸收过程中的细胞内pH调节

Regulation of intracellular pH during H+-coupled oligopeptide absorption in enterocytes from guinea-pig ileum.

作者信息

Hayashi H, Suzuki Y

机构信息

Laboratory of Physiology, School of Food and Nutritional Sciences, University of Shizuoka, 52-1 Yada, Shizuoka 422-8526, Japan

出版信息

J Physiol. 1998 Sep 1;511 ( Pt 2)(Pt 2):573-86. doi: 10.1111/j.1469-7793.1998.573bh.x.

Abstract
  1. The mechanisms for regulating the intracellular pH (pHi) level during oligopeptide absorption were investigated in the enterocytes from guinea-pig ileum by identifying the acid-base transporters responsible for extruding H+ that enters the cell through the H+-oligopeptide cotransporter. 2. The pHi level was measured by microfluorometry in an isolated villus tip loaded with the pH-sensitive fluoroprobe 2'7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). The oligopeptide-induced increment in the short-circuit current (Isc) was determined in a mucosal sheet in Ussing chambers. A CO2/HCO3--buffered solution was used. 3. The superfusion of glycylglycine (Gly-Gly, l0 mM) caused a decrease in pHi level, which returned to the basal level after removing Gly-Gly. This pHi recovery was strongly dependent on extracellular Na+. Amiloride partially inhibited the pHi recovery rate with an IC50 value of 41 microM, the maximum inhibition being approximately 70%. In the presence of amiloride at its maximum concentration (0.3 mM), the addition of 0.6 mM DIDS caused a further decrease, but did not abolish the pHi recovery rate. In the absence of CO2 and HCO3-, the pHi recovery was almost completely abolished by 0.3 mM amiloride. 4. The intracellular H+ accumulation induced by 0.3 mM amiloride or by 0.6 mM DIDS, as estimated from the pHi decrease and buffer capacity, was significantly greater during Gly-Gly superfusion than under resting conditions. 5. The increase in Isc induced by luminal glycylproline was attenuated by either removing serosal Na+ or by adding 0.5 mM amiloride or 0.6 mM DIDS to the serosal side. 6. We conclude that both Na+-dependent, amiloride-sensitive acid extrusion, probably by the Na+-H+ exchanger, and Na+- and HCO3--dependent, DIDS-sensitive acid extrusion, possibly by the Na+-HCO3- cotransporter, are involved in extruding H+ that enters cells by the H+-oligopeptide cotransport. It is proposed that these acid extrusion (or base loading) mechanisms are present in the basolateral membrane and are important for maintaining oligopeptide absorption, as well as the acid extrusion mechanism in the apical membrane.
摘要
  1. 通过鉴定负责排出通过H⁺ - 寡肽共转运体进入细胞的H⁺的酸碱转运体,研究了豚鼠回肠肠细胞在寡肽吸收过程中调节细胞内pH(pHi)水平的机制。2. 通过微量荧光测定法在装载有pH敏感荧光探针2'7'-双(2 - 羧乙基)-5(6)-羧基荧光素(BCECF)的分离绒毛尖端测量pHi水平。在Ussing室的黏膜片中测定寡肽诱导的短路电流(Isc)增加。使用CO₂/HCO₃⁻缓冲溶液。3. 灌注甘氨酰甘氨酸(Gly - Gly,10 mM)导致pHi水平降低,去除Gly - Gly后恢复到基础水平。这种pHi恢复强烈依赖于细胞外Na⁺。氨氯吡咪以41 microM的IC50值部分抑制pHi恢复率,最大抑制约为70%。在氨氯吡咪最大浓度(0.3 mM)存在下,添加0.6 mM DIDS导致进一步降低,但未消除pHi恢复率。在没有CO₂和HCO₃⁻的情况下,0.3 mM氨氯吡咪几乎完全消除了pHi恢复。4. 根据pHi降低和缓冲能力估计,0.3 mM氨氯吡咪或0.6 mM DIDS诱导的细胞内H⁺积累在Gly - Gly灌注期间比在静息条件下明显更大。5. 去除浆膜侧Na⁺或在浆膜侧添加0.5 mM氨氯吡咪或0.6 mM DIDS可减弱管腔甘氨酰脯氨酸诱导的Isc增加。6. 我们得出结论,Na⁺依赖性、氨氯吡咪敏感的酸排出,可能通过Na⁺ - H⁺交换器,以及Na⁺和HCO₃⁻依赖性、DIDS敏感的酸排出,可能通过Na⁺ - HCO₃⁻共转运体,都参与排出通过H⁺ - 寡肽共转运进入细胞的H⁺。提出这些酸排出(或碱加载)机制存在于基底外侧膜中,对于维持寡肽吸收以及顶端膜中的酸排出机制很重要。

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