Transport of sulphate in rat jejunal and rat proximal tubular basolateral membrane vesicles

Abstract

Basolateral membrane vesicles were isolated by a Percoll density gradient centrifugation method from small intestinal and renal proximal tubular epithelial cells. Transport of sulphate across the basolateral membrane was analyzed by measuring the uptake of tracer sulphate. In both membrane preparations, preloading the vesicles with sulphate- or hydroxyl-anions stimulated tracer sulphate uptake (trans-stimulation); an inwardly directed sodium gradient did not stimulate sulphate influx whether in the absence or in the presence of sulphate- or hydroxyl-ion-trans-stimulation. Under sulphate trans-stimulation conditions, DIDS (10(-4) mol/l) inhibited sulphate influx. In intestinal membranes, trans-stimulation of sulphate influx was obtained by preloading the vesicles with chloride, in renal membranes by preloading with bicarbonate. Under sulphate trans-stimulation conditions, in intestinal membranes, sulphate influx was strongly inhibited by chloride, in renal membranes, chloride inhibition was absent. Under bicarbonate trans-stimulation conditions, in renal membranes, sulphate transport was inhibited by lactate. It is concluded that small intestinal and renal proximal tubular basolateral membrane vesicles contain a transport mechanism for sulphate that cannot be energized by a sodium gradient. The transport system in small intestinal basolateral membranes seems to be different from that in renal membranes. It is suggested that the observed interaction between inorganic and organic anion transport in renal basolateral membranes is indirect.

Taurocholate transport by rat intestinal basolateral membrane vesicles. Evidence for the presence of an anion exchange transport system.

“…The presence of an anion exchange transporter in renal and intestinal basolateral membrane vesicles has been demonstrated using radiolabeled sulfate as a substrate (15,25,26). A characteristic ofthis transporter is that it can be driven additionally by a transmembrane pH difference (15).…”

Physiological Roles of Mammalian Sulfate Transporters NaS1 and Sat1

“…-dependent sulfate transporter (Schneider et al 1984;Turner 1984;Ullrich et al 1980), which was inhibited by thiosulfate, molybdate, chromate and selenate (Ullrich et al 1980). Renal proximal tubular BLM vesicles characterized a sulfate anion exchanger, that transports sulfate out of the cell (into the systemic circulation) and exchanges sulfate with thiosulfate, hydroxyl ions, bicarbonate, oxalate and a variety of organic ions and was inhibited by stilbene derivatives DIDS (4,4 0 -diisothiocyanato-2,2 0 -disulfonate) and SITS (4-acetamido-4 0 -isothiocyanato-2,2 0 -disulfonate) (Bastlein and Burckhardt 1986;Brazy and Dennis 1981;Hagenbuch et al 1985;Low et al 1984;Pritchard and Renfro 1983).…”

Ontogeny of renal sulfate transporters: postnatal mRNA and protein expression

“…This procedure gave an enrichment of 12.8±1.6-fold for the BBM marker enzymes maltase and leucine aminopeptidase, compared with a 1.2±0.4-fold enrichment for the basolateral membrane (BLM) marker enzyme Na-K-ATPase. Rat renal BLMs were isolated as previously described [27] and provided an enrichment of 807 the BLM marker Na-K-ATPase of 20.8±2.4-fold. Protein concentrations of the final BBM and BLM preparations were determined according to the Lowry method [28].…”