Acetazolamide inhibition of basolateral base exit in rabbit renal proximal tubule S2 segment |
| |
Authors: | G. Seki E. Frömter |
| |
Affiliation: | (1) Zentrum der Physiologie, J.W. Goethe Universität, Theodor-Stern-Kai 7, W-6000 Frankfurt/Main 70, Federal Republic of Germany;(2) Max-Planck-Institut für Biophysik, Kennedyallee 70, W-6000 Frankfurt/Main 70, Federal Republic of Germany |
| |
Abstract: | The influence of the carbonic anhydrase inhibitor acetazolamide (ACZ) was investigated on HCO3–transport mechanisms in the basolateral cell membrane of rabbit renal proximal tubule. Experiments were performed on isolated S2 segments using double-barrelled microelectrodes to measure cell membrane potential (Vb) and cell pH (pHi) during step changes in bath perfusate ion concentrations. Peritubular application of ACZ (1 mmol/l) reduced the initial Vb response to 101 reduction of bath HCO3–concentration only slightly, from +53.8±4.2 mV to+49.1±0.3 mV (n=5), but caused an intermittent overshooting repolarization in the secondary Vb response. In conjunction with these effects it left the initial pHi response virtually unchanged but induced a secondary slow acidification. These observation indicate that — under the present experimental conditions — ACZ does not block the Na+-HCO3–cotransporter but acts via inhibition of cytosolic carbonic anhydrase. This was confirmed by studying the effect of elevated intracellular HCO3–concentrations under reduced flux conditions and by comparing the concentration dependence of the Vb response with the inhibition kinetics of cytosolic carbonic anhydrase. In contrast, peritubular ACZ inhibited Na+-independent Cl–/HCO3–exchange in the basolateral cell membrane of S2 segments directly in a similar way to that described in the preceding publication for S3 segments. |
| |
Keywords: | Renal proximal tubule S2 segment Rheogenic Na+-HCO3– cotransport Cl– /HCO3– exchange Carbonic anhydrase inhibitor |
本文献已被 SpringerLink 等数据库收录! |
|