Stimulation by HCO 3 − of Na+ transport in rabbit gallbladder

Abstract

Bicarbonate presence in the bathing media doubles Na+ and fluid transepithelial transport and in parallel significantly increases Na+ and Cl- intracellular concentrations and contents, decreases K+ cell concentration without changing its amount, and causes a large cell swelling. Na+ and Cl- lumen-to-cell influxes are significantly enhanced, Na+ more so than Cl-. The stimulation does not raise any immediate change in luminal membrane potential and cannot be due to a HCO3(-)-ATPase in the brush border. The stimulation goes together with a large increase in a Na+-dependent H+ secretion into the lumen. All of these data suggests that HCO3- both activates Na+--Cl- cotransport and H+--Na+ countertransport at the luminal barrier. Thiocyanate inhibits Na+ and fluid transepithelial transport without affecting H+ secretion and HCO3(-)-dependent Na+ influx. It reduces Na+ and Cl- conentrations and contents, increases the same parameters for K+, causes a cell shrinking, and abolishes the lumen-to-cell Cl- influx. It enters the cell and is accumulated in the cytoplasm with a process which is Na+-dependent and HCO3(-)-activated. Thus SCN- is likely to compete for the Cl- site on the cotransport carrier and to be slowly transferred by the cotransport system itself.

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: I. Na+/H+, Cl−/HCO 3 − double exchange and Na+−Cl− symport

“…Experiments were designed based on the knowledge that no C1-conductance exists at the apical membrane of rabbit gallbladder Cremaschi & Meyer, 1982). Moreover, total cellular C1-influx is Na+-dependent (Cremaschi & Hrnin, 1975;Cremaschi, H6nin & Meyer, 1979;Cremaschi et al, 1983) and inhibited by SCN- (Cremaschi et al, 1979(Cremaschi et al, , 1983.…”

Bicarbonate effects, electromotive forces and potassium effluxes in rabbit and guinea‐pig gall‐bladder.

“…All this indicates, for both species, an increased dissociation of polyelectrolytes from protons, which is mainly compensated with free K+ concentration in the guinea-pig and with bound Na+ in the rabbit. Previous results obtained in the rabbit (Cremaschi & Henin, 1975a;Cremaschi et al 1979) also indicated that only a fraction of cellular Na+ was rapidly exchangeable with 22Na.…”

“…It is noteworthy that, in spite of the fact that HCO3-does not affect the apical conductive Na+ pathways, it significantly diminishes the apical electromotive force because of the decrease in the cell K+ activity it elicits and because of the dominant conductance of this cation at both cell aspects (Henin & Cremaschi, 1975;Cremaschi & Henin, 1975a). Thus, in the rabbit the apical electromotive force (Em), calculated (Cremaschi & Henin 1975a, b;Cremaschi et al 1979). More precisely K+ concentration is 184-1 ±4-5 mm (5) and 117-2 + 5-4 mm (13); Na+ concentration is 6-6 + 2-1 mm (5) and 58-7 + 4.9 mm (11).…”

“…No anion conductance is present in the apical membrane of rabbit gall-bladder (HWnin & Cremaschi, 1975;Cremaschi et al 1979;Cremaschi & Meyer, 1982); conversely, it is substantial in the guinea-pig (Cremaschi & Meyer, 1982). The following series of experiments was programmed to discriminate whether it is due in this animal to Cl-or HCO3-or both anions.…”

Proceedings of the Physiological Society and the Societa Italiana Di Fisiologia, 11‐13 July 1985, Oxford Meeting: Poster Communications

“…Only 42 + 05 nequiv cm-2 h-1 (13 exp.) were SCN--and Na+-insensitive (junctional component; Cremaschi & Henin, 1975;Cremaschi, Henin & Meyer, 1979;Cremaschi et al 1983). At maximal effects 10-3 M-amiloride, 10-4 M-SITS and 5-5 x 10-5 M furosemide only about halved the cellular component of Cl-influx (SCN--and Na+-sensitive).…”