On the mechanism of bicarbonate exit from renal proximal tubular cells.
On the mechanism of bicarbonate exit from renal proximal tubular cells.
复制标题
关于碳酸氢盐从肾近端肾小管细胞排出的机制。
DOI:
--
复制
发表时间:
1996
影响因子:
19.6
通讯作者:
Eberhard Frömter
中科院分区:
文献类型:
--
作者:
G. Seki;Salvatore Coppola;K. Yoshitomi;B.;I. Samaržija;S. Müller;Eberhard Frömter
We compare here the results of electrophysiological measurements on proximal tubular cells performed on rat kidney in vivo and on isolated rabbit and rat tubules in vitro. Based on different effects of carbonic anhydrase inhibitors in the in vivo and in vitro preparation, we conclude that NaHCO3 cotransport across the basolateral cell membrane functions as Na(+)-CO3(2-)-HCO3- cotransport in vivo, but as Na(+)-HCO3(-)-HCO3- cotransport in the classical in vitro preparation. The former, but not the latter, transport mode is characterized by generation of local disequilibrium pH/CO3(2-) concentrations that oppose fluxes if membrane-bound carbonic anhydrase is inhibited. In support of this conclusion, we find that overall transport functions with a HCO3- to Na+ stoichiometry of 3:1 in vivo (since each transported CO3(2-) eventually generates 2 HCO3- ions), but 2:1 in vitro. This has been deduced from various measurements, among them super-Nernstian and reverse nernstian, potential responses to changing ion concentrations which are characteristic of obligatorily coupled cation-anion cotransporters, but are not known in classical electrochemistry. The different transport modes in vivo and in vitro suggest that isolated proximal tubules have functional deficits compared to proximal tubules in vivo.
DOI:
10.1172/jci113980
发表时间:
1989-03
期刊:
The Journal of clinical investigation
影响因子:
--
作者:
M. Soleimani;P. Aronson
通讯作者:
M. Soleimani;P. Aronson
DOI:
10.1016/s0021-9258(18)51463-0
发表时间:
1989-11
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
M. Soleimani;P. Aronson
通讯作者:
M. Soleimani;P. Aronson