## Abstract

The cellular mechanism of active chloride secretion, as it is manifested in the intestine and trachea, appears to possess the following elements: (1) NaCl co-transport across the basolateral membrane; (2) Cl<latex>$^-$</latex> accumulation in the cell above electrochemical equilibrium due to the Na<latex>$^+$</latex> gradient; (3) a basolateral Na<latex>$^+$</latex>-K<latex>$^+$</latex> pump that maintains the Na<latex>$^+$</latex> gradient; (4) a hormone-regulated Cl<latex>$^-$</latex> permeability in the apical membrane; (5) passive Na<latex>$^+$</latex> secretion through a paracellular route, driven by the transepithelial potential difference; and (6) an increase in basolateral membrane K<latex>$^+$</latex> permeability occurring in conjunction with an increase in Na<latex>$^+$</latex>-K<latex>$^+$</latex> pump rate. Electrophysiological studies in canine trachea support this model. Adrenalin, a potent secretory stimulus in that tissue, increases apical membrane conductance through a selective increase in Cl<latex>$^-$</latex> permeability. Adrenalin also appears to increase basolateral membrane K<latex>$^+$</latex> permeability. Whether or not adrenalin also increases paracellular Na<latex>$^+$</latex> permeability is unclear. Some of the testable implications of the above secretion model are discussed.