In the unstimulated oxyntic (or parietal) cell, the primary pump for g
astric HCl secretion, the H+/K+-ATPase, is retained within the cytopla
sm in a membranous compartment of tubulovesicles. Neural or hormonal s
timulation of acid secretion induces extensive membrane transformation
s consistent with a fusion and recruitment of tubulovesicles to the ap
ical plasma membrane. The consequent placement of H+/K+-ATPase in para
llel with K+ and Cl- channels provides the necessary ionic flow and AT
P-driven exchange for Met HCl secretion. Current evidence is consisten
t with a recruitment and recycling of membrane transporters, such as H
+/K+-ATPase, through docking/fusion machinery analogous to that in man
y other systems.