title: Plasticity of intercalated cell polarity: effect of metabolic acidosis.
abstract: The cortical collecting duct (CCD) is capable of secreting H(+) or HCO3(-) depending on the acid-base status in vivo. Transport is a function of two types of intercalated cells in the CCD: A-intercalated cells secrete H(+) and B-intercalated cells secrete HCO3(-). Metabolic acidosis results in a decrease in HCO3(-) secretion and an increase in H(+) secretion by the respective cells. Using a model of metabolic acidosis in vitro, we have shown that the down-regulation of HCO3(-) secretion occurs by endocytosis of apical anion exchangers in B-intercalated cells. The finding of basolateral anion exchangers in some adapted B-intercalated cells is consistent with a reversal of functional epithelial polarity. Plasticity of polarity is also observed in cultured intercalated cells: high-density plating results in converting B- to A-intercalated cells via the deposition of the novel protein hensin in the extracellular matrix. A key problem in renal physiology is to investigate the role of hensin in mediating the adaptation of the CCD to acidosis in vitro and in vivo.
authors: Department of Pediatrics, University of Rochester School of Medicine, Rochester, NY 14642, USA. George_Schwartz@urmc.rochester.edu
authors: G J
authors: GJ
authors: Schwartz
mesh_terms: D000138:Acidosis / Q000503:physiopathology*; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D016764:Cell Polarity / Q000502:physiology*; D004705:Endocytosis; D006801:Humans; D007672:Kidney Cortex / Q000166:cytology / Q000502:physiology* / Q000503:physiopathology; D007685:Kidney Tubules, Collecting / Q000166:cytology / Q000502:physiology* / Q000503:physiopathology
chemical_list: D001639:Bicarbonates