• DOI:10.1152/AJPCELL.1997.272.4.C1211
• Corpus ID: 44494678

A caffeine-sensitive Ca2+ store modulates K+-evoked secretion in chromaffin cells.

@article{Lara1997ACC,
  title={A caffeine-sensitive Ca2+ store modulates K+-evoked secretion in chromaffin cells.},
  author={Baldomero Lara and M. G. L{\'o}pez and M{\'e}rcedes Villarroya and Luis Gand{\'i}a and L. Cleeman and M. Morad and A. G. Garcı́a},
  journal={The American journal of physiology},
  year={1997},
  volume={272 4 Pt 1},
  pages={
          C1211-21
        }
}

• B. Lara, M. G. López, +4 authors A. Garcı́a
• Published 1 April 1997
• Biology
• The American journal of physiology

Catecholamine release from bovine adrenal medulla chromaffin cells superfused with a Krebs-N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid solution was monitored on-line with an electrochemical detector. Caffeine (10 mM) progressively depressed the magnitude of secretory responses to depolarizing pulses of 70 mM K+ and 2 mM Ca2+ (70 K+/2 Ca2+) in cells superfused with a Krebs-N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid solution containing 0 mM Ca2+ + 0.5 mM EGTA; blockade reached 80% at the third 70 K+/2 Ca2+ challenge given in the presence of caffeine. A similar effect was obtained when, instead of continuous superfusion, prepulses of caffeine were applied (10 mM for 60 s). The blocking effects of caffeine on K+-induced secretion depended on the time of exposure to the drug: the longer the exposure time the greater the blockade. The recovery of the K+ secretory responses previously impaired by caffeine was always gradual and followed a staircase mode. This contrasts with the effects of caffeine on various parameters measuring Ca2+ entry through Ca2+ channels, which did not parallel its effects on K+-evoked secretion. The secretion data, however, are compatible with the disappearance and recovery of an intracellular Ca2+ concentration signal triggered by K+ in single chromaffin cells loaded with fura 2 and treated with 10 mM caffeine. Thus, contrary to previous views, the depression of secretion by caffeine does not seem to be associated with inhibition of extracellular Ca2+ entry through Ca2+ channels. These functional data are, rather, compatible with the view that the degree of filling of a caffeine-sensitive intracellular Ca2+ store might regulate the extent of exocytosis. When emptied, such a store might act as a sink for the external Ca2+ entering through Ca2+ channels during cell depolarization, thus decreasing the intracellular Ca2+ concentration available for exocytosis.