AJP - Cell Physiology, Vol 258, Issue 1 C147-C155, Copyright © 1990 by American Physiological Society

ARTICLES

Oscillatory mode of calcium signaling in rat pancreatic acinar cells

Y. Tsunoda, E. L. Stuenkel and J. A. Williams
Department of Physiology, University of Michigan, Ann Arbor 48109.

Cytoplasmic free calcium concentration ((Ca2+]i) was evaluated by dual-wavelength microspectrofluorometry of fura-2-loaded individual rat pancreatic acinar cells. Resting [Ca2+]i in unstimulated acini was 94.1 +/- 4.1 nM. Stimulation with high concentrations of cholecystokinin (CCK, 100 pM to 1 nM) led to an immediate rise in [Ca2+]i to 400-1,000 nM followed by a fall within 2-5 min to a plateau only slightly above the prestimulation level. Lower and more physiological concentrations of CCK (1-30 pM), after a latent period of 60-90 s, induced a smaller sustained increase in [Ca2+]i (30-40 nM) with superimposed repetitive transient [Ca2+]i spikes. These oscillations averaged 120-150 nM in amplitude, occurred at a frequency which averaged 1.5 times/min, and were maintained as long as the stimulus was applied. Similar [Ca2+]i oscillations were observed when acini were stimulated with submaximal concentrations of carbamylcholine (0.1-1 microM) and neuromedin C (0.1-1 nM). Intracellular Ca2+ stores were not depleted during [Ca2+] oscillations, since a subsequent increase to 1 nM CCK led to an immediate rise in [Ca2+]i indistinguishable from the response of cells initially stimulated at this concentration. Although extracellular Ca2+ was required for maintenance of frequency of the spikes, the major source of Ca2+ utilized for oscillations was intracellular, since elimination of medium Ca2+ or Ca2+ entry blockade with lanthanum failed to inhibit oscillations. Vasoactive intestinal polypeptide (10 nM) and high K+ (50 mM) did not affect [Ca2+]i oscillations. Antimycin (10 microM), which depletes cytoplasmic ATP, increased basal [Ca2+]i and inhibited the oscillations.(ABSTRACT TRUNCATED AT 250 WORDS)

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