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A fundamental element of acid-base regulation is the ability of the kidney to respond to changes in dietary acid composition by modifying rates of net acid excretion. A key component of this homeostatic response was first demonstrated by McKinney and Burg (1), who examined net H 1 /HCO transport in rabbit cortical collecting ducts removed from the in vivo milieu and perfused in vitro. In vitro perfused cortical collecting ducts from rabbits ingesting an acid diet secreted H 1 into the luminal fluid, whereas cortical collecting ducts from animals ingesting an alkaline diet secreted HCO . This finding represented an example of long term memory in renal epithelial cells, wherein the in vivo milieu determined cellular behavior in vitro. The cortical collecting duct is composed of three cell types, a principal cell which does not contribute to H 1 /HCO transport, an a -intercalated cell which secretes H 1 into the lumen, and a b -intercalated cell which secretes HCO into the lumen. In a -intercalated cells H 1 secretion is mediated by an apical membrane vacuolar H 1 pump and a basolateral membrane Cl 2 /HCO exchanger, whereas in b -intercalated cells HCO secretion is mediated by similar transporters with reversed polarity, a basolateral membrane vacuolar H 1 pump, and an apical membrane Cl 2 /HCO exchanger. However, in a -intercalated cells the basolateral membrane Cl 2 /HCO exchanger is encoded by the AE1 gene, whereas in b -intercalated cells the apical Cl 2 /HCO exchanger does not label with antibodies against AE1. Roles for an H,K-ATPase in these processes have been proposed but have not been established. Schwartz et al. (2) found that a -intercalated cells demonstrate apical endocytosis whereas b -intercalated cells exhibit basolateral membrane endocytosis; in both cases endo/exocytosis was proposed to mediate trafficking of the vacuolar H 1 pump to and from the plasma membrane. Using apical endocytosis as a marker for a -intercalated cells, Schwartz et al. (2) found that administration of acid to rabbits caused an increase in the number of a -intercalated cells with a decrease in the number of b -intercalated cells and no change in the total number of intercalated cells. In addition, it was noted that this transition occurred in the absence of mitosis, suggesting that it involved an adaptive change in cell function rather than proliferation and death of specific cell types. Based on these results, it was proposed that this adaptation involved a transition of b to a -intercalated cells, possibly a reversal of epithelial polarity wherein the apical membrane Cl 2 / HCO exchanger moved to the basolateral membrane and the basolateral membrane vacuolar H 1 pump moved to the apical membrane (2). Subsequent studies using markers similar to those described above, have found that intercalated cells can be divided into more than two subtypes, and that the response to acid may be more complicated than a mere interconversion between a and b -intercalated cells. Nevertheless, a significant adaptation in intercalated cell function and morphology oc3 2

Hensin: a matrix protein determinant of epithelial polarity.