CHLORIDE CONDUCTANCES OF SALT-SECRETING EPITHELIAL-CELLS

There has been much interest in apical membrane receptors for regulatory substances released from immune cells. Chloride conductance pathways at the apical membranes of epithelial cells play a well-defined role in determining the rate of salt secretion across the epithelia. Salt secretion is regulated on the seconds–minutes time scale by a variety of endocrine substances, neurotransmitters, and immune cell products, whose receptors lie predominantly at the plasma-facing, basolateral membranes. Secretion can be activated also by bacterial enterotoxins, acting from the lumen, for example, those inducing intestinal secretion and diarrhea. It is evident that Cl conductance in secretory cells has been identified at a variety of levels of resolution. The role of secondary-active Cl transport in salt secretion has been identified, from transepithelial measurements, and the location of Cl conductances at the apical membranes is resolved, using microelectrode recordings. The introduction of single-channel recording techniques generated candidates for the apical membrane secretory Cl channel. However, the leap from the Ussing chamber to the patch pipette left in its wake considerable uncertainty, as to the single-channel basis of the regulated Cl conductance pathways of secretory epithelial cells. Ultimately, whole-cell recording techniques bridged this gap and identified three regulated Cl current components, two of which are controlled by secretory agonists, the other by cell volume. The primary signal transduction events that control the activities of the secretory Cl conductance have emerged, but the understanding of their detailed modulation is incomplete. © 1994 Academic Press, Inc.