Calcium reduces the sodium permeability of luminal membrane vesicles from toad bladder. Studies using a fast-reaction apparatus.

Abstract

Regulation of the sodium permeability of the luminal membrane is the major mechanism by which the net rate of sodium transport across tight epithelia is varied. Previous evidence has suggested that the permeability of the luminal membrane might be regulated by changes in intracellular sodium or calcium acti¥ities. To test this directly, we isolated a fraction of the plasma membrane from the toad urinary bladder, which contains a fast, amiloridesensitive sodium flux with characteristics similar to those of the native luminal membrane. Using a flow-quench apparatus to measure the initial rate of sodium efflux from these vesicles in the millisecond time range, we have demonstrated that the isotope exchange permeability of these vesicles is very sensitive to calcium. Calcium reduces the sodium permeability, and the half-maximal inhibitory concentration is 0.5 #M, well within the range of calcium activity found in cells. Also, the permeability of the luminal membrane vesicles is little affected by the ambient sodium concentration. These results, when taken together with studies on whole tissue, suggest that cell calcium may be an important regulator of transepithelial sodium transport by its effect on luminal sodium permeability. The effect of cell sodium on permeability may be mediated by calcium rather than by sodium itself.

Direct inhibition of epithelial Na+ channels by a pH-dependent interaction with calcium, and by other divalent ions

“…In agreement with a previous report (Chase & A1-Awqati, 1983) we found that including submicromolar concentrations of free Ca 2+ in the vesicles, substantially lowers the channel-mediated flux. These results appear, however, to be different from those obtained recently using rat collecting tubules (Palmer & Frindt, 1986).…”

Physiological role of apical potassium ion channels in frog skin.

“…Therefore, we attempted to manipulate the intracellular Ca2+ concentration in a different way, by removal of Na+ from the serosal solution. Recently, the presence of a Na+/Ca2+ exchange mechanism at the basolateral membrane offrog skin (Grinstein & Erlij, 1978) and toad bladder (Chase & Al-Awqati, 1983) has been demonstrated. This transport system is responsible for the extrusion of Ca2+ from the cytosolic compartment and operates through the inward-oriented driving force for Na+.…”

Relation between intracellular sodium and active sodium transport in rabbit colon: Current-voltage relations of the apical sodium entry mechanism in the presence of varying luminal sodium concentrations

“…Evidence has been presented for the presence of a Na-Ca countertransport mechanism at the basolateral membranes of toad (Chase & A1-Awqati, 1983 ;Arruda et al, 1982) and turtle urinary bladder (Arruda, Sabatini & Westenfelder, 1982), rat small intestine (Hildmann, Schmidt & Murer, 1982), Necturus renal proximal tubule (Lee, Taylor & Windhager, 1980), and frog skin (Grinstein & Erlij, 1978) whereby the movement of Na into the cell across the basolateral membrane energizes the uphill extrusion of Ca from the cell across that barrier. If, as in other tissues (Blaustein, 1974), this mechanism is rheogenic involving the counterflow of more than 2 Na per Ca, the driving force for Ca extrusion is derived from both the Nachemical gradient and the electrical potential difference across that membrane.…”