White J F, Imon M A
Am J Physiol. 1981 Nov;241(5):G389-96. doi: 10.1152/ajpgi.1981.241.5.G389.
Isolated segments of jejunum from Amphiuma bathed in Cl--free (SO42(-)) media usually generated serosa-negative electrical potentials when HCO3(-) was present in the media. Bidirectional isotope fluxes under short circuit revealed a negligible absorption of Na+ and a residual flux consistent with anion absorption. Acetazolamide (10(-4) M) eliminated the short-circuit current and the residual flux. Segments of jejunum exposed on the mucosal surface to HCO3(-) (pH 7.4) alkalinized the unbuffered serosal fluid at a rate of about 1.1 mueq . h-1 . cm-2, as measured by the pH-stat while clamped at zero transepithelial potential. Acetazolamide, anoxia, and 2,4-dinitrophenol lowered the rate of alkalinization and simultaneously reduced the short-circuit current by an equal amount. Absorption was constant above a [HCO3(-)] of 35 meq/l and uninfluenced by applied transepithelial voltage gradients. HCO3(-) absorption was not reduced after replacement of media Na+ or Cl- but was reduced on addition of ouabain or removal of K+. It is concluded that the jejunum actively absorbs HCO3(-) by an electrogenic process that does not involve Na+-H+ exchange.
将钝口螈空肠的分离节段置于无 Cl⁻(SO₄²⁻)的培养基中培养时,若培养基中存在 HCO₃⁻,通常会产生浆膜负电位。短路条件下的双向同位素通量显示,Na⁺的吸收可忽略不计,且存在与阴离子吸收一致的残余通量。乙酰唑胺(10⁻⁴ M)消除了短路电流和残余通量。将空肠节段的黏膜表面暴露于 HCO₃⁻(pH 7.4)中,通过 pH 计在跨上皮电位为零时测量发现,未缓冲的浆膜液以约 1.1 μeq·h⁻¹·cm⁻²的速率碱化。乙酰唑胺、缺氧和 2,4 - 二硝基苯酚降低了碱化速率,同时使短路电流等量降低。当[HCO₃⁻]高于 35 meq/L 时,吸收恒定,且不受施加的跨上皮电压梯度影响。培养基中 Na⁺或 Cl⁻被替代后,HCO₃⁻的吸收并未降低,但加入哇巴因或去除 K⁺后,吸收降低。得出的结论是,空肠通过一种不涉及 Na⁺ - H⁺交换的电生过程主动吸收 HCO₃⁻。