Na+/myo-inositol transport is regulated by basolateral tonicity in Madin-Darby canine kidney cells.

AUTOR(ES)

Yamauchi, A

RESUMO

We investigated the effects of change in basolateral osmolality on Na(+)-dependent myo-inositol uptake in Madin-Darby canine kidney cells to test our hypothesis that the Na+/myo-inositol transporter (SMIT), an osmolyte transporter, is mainly regulated by osmolality on the basolateral surface. A significant osmotic gradient between both sides of the epithelium persisted at least 10 h after basolateral osmolality was increased. [3H]myo-inositol uptake increased in a basolateral osmolality-dependent manner. The magnitude of the increase is comparable to that for making both sides hypertonic. Apical hypertonicity also increased the uptake on the basal side, but the magnitude of the increase was significantly smaller than the basolateral or both sides hypertonicity. Betaine-gamma-amino-n-butyric acid transporter activity, measured by [3H]gamma-amino-n-butyric uptake, showed a pattern similar to SMIT activity in response to basolateral hypertonicity. The most plausible explanation for the polarized effect of hypertonicity is that the basal membrane is much more water permeable than the apical membrane. These results seem to be consistent with the localization and regulation of the SMIT in vivo.

Documentos Relacionados

• Taurine behaves as an osmolyte in Madin-Darby canine kidney cells. Protection by polarized, regulated transport of taurine.
• TGN38 recycles basolaterally in polarized Madin-Darby canine kidney cells.
• Differential localization of syntaxin isoforms in polarized Madin-Darby canine kidney cells.
• Spontaneously oscillating K+ channel activity in transformed Madin-Darby canine kidney cells.
• Bradykinin-activated membrane-associated phospholipase C in Madin-Darby canine kidney cells.