Heintze K, Petersen K U, Wood J R
J Membr Biol. 1981;62(3):175-81. doi: 10.1007/BF01998163.
The effect of bicarbonate (HCO3) on fluid absorption by guinea pig gallbladder was investigated in vitro. Stimulation of fluid absorption was concentration dependent resulting in a fourfold increase in transport over the range 1 to 50 mM. Phosphate, Tris, glycodiazine and glutamine buffers failed to substitute for HCO3 in stimulating absorption. Unidirectional 22Na fluxes were measured across short-circuited sheets of guinea pig and rabbit gallbladders mounted in Ussing-type chambers. In both species the net Na flux was unaffected by serosal HCO3 alone but was stimulated by addition of HCO3 to the mucosal bathing solution. Transepithelial electrical potential difference in rabbit gallbladder was about 1.4 mV (lumen positive) when HCO3 was present in the mucosal or in both compartments. This fell to 0.2 mV under HCO3-free conditions or when HCO3 was present only in the serosal solution. The respective values for guinea pig gallbladder were -1.6 and -0.6 mV (lumen negative). HCO3 stimulation of Na absorption by guinea pig gallbladder was abolished by increasing the bathing pH from 7.4 to 7.8, an effect resulting mainly from a reduction in JNams. Tris buffer (25 mM) inhibited HCO3-dependent fluid absorption in this species completely at pH 8.5 and partially at 7.5. These results indicate that HCO3 stimulates gallbladder transport in both species by an action from the mucosal side. This effect cannot be attributed to simple buffering of H+ but may be explained by the participation of HCO3 in the maintenance of intracellular H+ for a Na/H-exchange.
在体外研究了碳酸氢盐(HCO₃)对豚鼠胆囊液体吸收的影响。液体吸收的刺激呈浓度依赖性,在1至50 mM范围内转运增加了四倍。磷酸盐、Tris、甘氨双唑啉和谷氨酰胺缓冲液在刺激吸收方面无法替代HCO₃。通过安装在Ussing型小室中的豚鼠和兔胆囊的短路薄片测量单向²²Na通量。在这两个物种中,净Na通量不受单独的浆膜HCO₃影响,但通过向黏膜浴液中添加HCO₃而受到刺激。当HCO₃存在于黏膜或两个隔室中时,兔胆囊的跨上皮电位差约为1.4 mV(腔面为正)。在无HCO₃条件下或当HCO₃仅存在于浆膜溶液中时,该电位差降至0.2 mV。豚鼠胆囊的相应值为-1.6和-0.6 mV(腔面为负)。将浴液pH从7.4提高到7.8可消除HCO₃对豚鼠胆囊Na吸收的刺激,这种效应主要是由于JNams降低所致。Tris缓冲液(25 mM)在pH 8.5时完全抑制该物种中HCO₃依赖性液体吸收,在pH 7.5时部分抑制。这些结果表明,HCO₃通过从黏膜侧的作用刺激两个物种的胆囊转运。这种效应不能归因于对H⁺的简单缓冲,而可能是由于HCO₃参与维持细胞内H⁺以进行Na⁺/H⁺交换来解释。