In the circular muscle of the guinea-pig gastric antrum, a decrease in the external Na+ to less than 20 mM produced depolarization of the membrane with transient prolongation of the slow wave. This was followed by a high rhythmic activity. The activity was inhibited by reapplication of Na+ before recovery. The depolarization in Na+-deficient solution was prevented and rhythmic activity continued at about 5/min for at least 6 min by simultaneous removal of K+, Ca2+, or Cl-. After exposure to a NA+- and Cl--deficient solution for a few minutes, reapplication of the Na+ in Cl--deficient solution inhibited generation of the slow wave until Cl- reapplication. Similar results were obtained when Na+ and Cl- were reapplied in the absence of K+ after exposure to a Na+-, K+-free, an Cl--deficient solution, although the inhibition was weaker than Na+ reapplication in a Cl--deficient solution. In the presence of furosemide or bumetanide, a strong inhibition of activity was produced by the reapplication of Na+ and Cl- after exposure to an Na+- and Cl--deficient solution. A hypothesis is presented that intracellular Ca2+ concentration ([Ca2+]i) is the most important factor determining the generation and frequency of the slow wave and that [Ca2+]i is regulated by the Na+ concentration gradient across the plasma membrane. The recovery of the Na+ concentration gradient by Na+ reapplication after removal of Na+ and Cl- is mainly controlled by a Na+-K+-Cl- co-transport.
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