Feldman G M
Department of Medicine, McGuire Veterans Affairs Medical Center, Richmond, Virginia.
Gastroenterology. 1994 Aug;107(2):329-38. doi: 10.1016/0016-5085(94)90156-2.
BACKGROUND/AIMS: The large intestine secretes HCO3- via a Cl-/HCO3- exchange mechanism located in the apical membrane of colonocytes. However, an additional transport system(s) must facilitate HCO3- (OH-) entry or H+ exit across the basolateral cell surface. The aim of this study was to determine that mechanism(s).
A modified Ussing apparatus was used to measure net HCO3- secretion in segments of rat distal colon.
When added to the serosal solution, 10 mmol/L 4-acetamido-4'-isothiocyano-2,2'-disulfonic acid stilbene (SITS), 1 mmol/L SITS and 0.1 mmol/L diisothiocyanostilbene-2,2'-disulfonic acid, inhibited HCO3- secretion by 88%, 51%, and 30%, respectively. However, the Na+/H+ exchange inhibitors, amiloride (1 mmol/L), dimethylamiloride (0.1 mmol/L), ethylisopropylamiloride (0.1 mmol/L), failed to affect HCO3- secretion. Acetazolamide (1 mmol/L) blocked HCO3- secretion by approximately 60% when in the serosal solution but had little effect when in the mucosal solution. Ion substitution studies showed that HCO3- secretion required Na+ in the serosal solution (K0.5 approximately 12 mmol/L). HCO3- secretion was unaffected by depolarizing the basolateral membrane potential with K(+)-rich medium.
These data are consistent with Na+ linked HCO3- transport across the colonocyte basolateral membrane, which appears to be electroneutral.
背景/目的:大肠通过位于结肠上皮细胞顶端膜的Cl⁻/HCO₃⁻交换机制分泌HCO₃⁻。然而,必须有其他转运系统促进HCO₃⁻(OH⁻)进入或H⁺穿过基底外侧细胞表面排出。本研究的目的是确定该机制。
使用改良的Ussing装置测量大鼠远端结肠段的净HCO₃⁻分泌。
当加入浆膜溶液时,10 mmol/L 4-乙酰氨基-4'-异硫氰基-2,2'-二磺酸芪(SITS)、1 mmol/L SITS和0.1 mmol/L二异硫氰基芪-2,2'-二磺酸分别抑制HCO₃⁻分泌88%、51%和30%。然而,Na⁺/H⁺交换抑制剂阿米洛利(1 mmol/L)、二甲基阿米洛利(0.1 mmol/L)、乙基异丙基阿米洛利(0.1 mmol/L)对HCO₃⁻分泌无影响。乙酰唑胺(1 mmol/L)在浆膜溶液中时可阻断约60%的HCO₃⁻分泌,但在粘膜溶液中时影响很小。离子替代研究表明,HCO₃⁻分泌需要浆膜溶液中有Na⁺(K0.5约为12 mmol/L)。用富含K⁺的培养基使基底外侧膜电位去极化对HCO₃⁻分泌无影响。
这些数据与Na⁺相关的HCO₃⁻跨结肠上皮细胞基底外侧膜转运一致,该转运似乎是电中性的。