Sodium-bicarbonate cotransport occurs in rat kidney cortical membranes but not in rat small intestinal basolateral membranes

Abstract

Basolateral membrane vesicles were isolated from rat kidney cortex and small intestinal enterocytes. Both membrane preparations show ATP-dependent calcium uptake and cytochalasin B-sensitive D-glucose transport. In renal membranes, sodium influx is stimulated by bicarbonate; bicarbonate-dependent sodium flux is membrane-potential-dependent and inhibited by 4,4'-di-isothiocyanato-2, 2'-stilbenedisulphanic acid ('DIDS'). Small intestinal basolateral membranes do not show bicarbonate-dependent sodium fluxes.

Cl/HCO3 exchange in the basolateral membrane domain of rat jejunal enterocyte

“…Data of Fig. 1 do not support the hypothesized mechanism, in agreement with previous studies carried out in this laboratory [11] and with more recent results presented by Hagenbuch et al [17]. These Authors suggested the possibility that a K-HCO3 cotransport could be involved in intestinal basolateral HCO3 exit, as proposed by Lucas [25] on the basis of electrophysiological measurements.…”

“…The sidedness of our basolateral membrane preparation was determined with latency of (Na,K)-ATPase and reported in a previous work [39]; after activation of (Na,K)-ATPase with the detergent sodium dodecylsulfate (SDS) we calculated that the ratio of unsealed to right-side-out to inside-out vesicles is 2 : 2 : 1. The first set of studies was designed to test for the presence of the transport system that achieves the greater part of basolateral HCO3 efflux in mammalian kidney, namely the sodium-bicarbonate cotransport [2,5,12,16,17,37,44]. As shown in Fig.…”

“…For this reason sucrose, which is a poorly permeating substance, could be used to increase osmolarity. In view of the presence of many similar transport mechanisms in renal and small intestinal basolateral membranes [27], we focused our attention on the Na-(HCO3)3 cotransport, which is the major basolateral membrane pathway for bicarbonate in the proximal tubule [2,5,12,16,17,37,44]. In our experimental conditions membrane potential was shunted by valinomycin and equal potassium concentrations in internal and external solutions; in order to maintain the imposed HCO3 concentration, experiments were performed at pH 8.2.…”

“…In the basolateral membrane domain of various epithelial tissues a number of anion transport systems have been described dealing with bicarbonate and chloride movements: C1/HCO3 exchange [3,13,16], Na-coupled C1/HCO3 exchange [3,14,16,33,37], electrogenic Na-(HCO3)3 cotransport [2,5,9,12,16,17,37,44], passive rheogenic bicarbonate transfer [4,6] and C1 conductance [20,35]. There is evidence that in several cell types anions cross basolateral membranes by means of multiple pathways [13,28,33].…”

Regulation of intracellular pH during H+‐coupled oligopeptide absorption in enterocytes from guinea‐pig ileum

“…Operation of the putative Na + ‐HCO 3 − cotransporter in the inward direction may facilitate H + ‐coupled, electrogenic oligopeptide influx not only due to the neutralization of accumulated H + , but possibly also due to the hyperpolarization of membrane potential, because most subtypes of the Na + ‐HCO 3 − cotransporter are known to transport more than one HCO 3 − with each Na + (Boron et al 1997). The presence of a Na + ‐HCO 3 − cotransporter has been suggested in intestinal cells from several species (Osypiw et al 1994; Peral et al 1995; Bernardo et al 1996; MacLeod et al 1996), although the basolateral membrane localization of a Na + ‐HCO 3 − cotransporter has not been described (Hagenbuch et al 1987; Tosco et al 1995). In many cell types, Na + ‐HCO 3 − cotransporters have been shown to be inhibited by DIDS (Boron et al 1997), although the Na + ‐HCO 3 − cotransporter in the crypt cells of the guinea‐pig has been suggested to be resistant to DIDS (MacLeod et al 1996).…”