Rapid Stimulation-Associated Changes in Exocrine Na⁺,K⁺-ATPase Subcellular Distribution

Many of the fluid-transporting epithelia sustain abrupt changes in Na⁺ entry rates during their normal daily patterns of activity. In the small intestine and in the gallbladder the rate of pumping by the basolateral membrane localized Na⁺,K'-ATPase increases to match increases in the rate of Na⁺ entry. As steady state cytosolic Na⁺ activities remain essentially unchanged, the cell must in some way be capable of sensing changes in the Na⁺ influx rate and adjusting the Na⁺K⁺-ATPase pump parameters appropriately. The mechanisms underlying this phenomenon of homocellular regulation remain largely matters of conjecture. Current concepts about the mechanism of NaCl secretion in exocrine gland acini suggest key roles for coupled Na⁺-CI^- entry and for Na ⁺, K⁺- ATPase-driven Na⁺ extrusion. As transepithelial flux rates and Na⁺ influx rates can change rapidly in response to increased levels of hormonal or neural stimulation, it seems likely that exocrine acinar cells also possess efficient homocellular mechanisms for regulating their cytosolic Na⁺ activities. The thesis of this chapter is that the recruitment of Na⁺, K⁺-ATPase pump units mobilized from preformed cytoplasmic pools is an important aspect of this process. The chapter begins by reviewing the roles of coupled Na⁺-C1^- influx mechanisms and of Na⁺,K⁺'-ATPase in exocrine secretion and by summarizing published evidence that a variety of cell types contain substantial cytoplasmic pools of Na⁺, K⁺-ATPase.