On the role of cellular calcium in the response of the parotid to dibutyryl and monobutyryl cyclic AMP.

The role of intracellular Ca in the exocytosis of α-amylase stimulated by derivatives of cyclic AMP was investigated. Partial depletion of cellular Ca stores was accomplished by prolonged (100–120 min) incubation in media containing no added Ca and 5.0 mM ethyleneglycolbis (aminoethylether)-N,N′-tetraacetic acid (EGTA). Release of α-amylase in response to the N⁶, O²′-dibutyryl or N⁶-monobutyryl derivatives of cyclic adenosine-3′,5′-monophosphate (cyclic AMP) was significantly inhibited by this procedure. When K⁺]° was increased from 5.0 mM to 25.0 mM, Ca-depletion was accelerated, as was the inhibition of the response to the monobutyryl derivative. The Ca-depletion regimen did not affect the cellular content of other cations, suggesting that the effects were specific for Ca. The effects of the cyclic AMP derivatives on release of Ca was also investigated. Both monobutyryl and dibutyryl cyclic AMP significantly enhanced the rate of release of ⁴⁵Ca from pre-loaded parotid slices. These observations lend support to the hypothesis previously set forth suggesting that in the parotid, cyclic AMP acts to release Ca from intracellular stores. It is this rise in cytosolic Ca which may catalyze the events ultimately leading to exocytosis.