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J. Biol. Chem., Vol. 269, Issue 17, 12438-12443, Apr, 1994

Heterogeneity between intracellular Ca2+ stores as the underlying principle of quantal Ca2+ release by inositol 1,4,5-trisphosphate in permeabilized pancreatic acinar cells

FH van de Put, JJ De Pont and PH Willems
Department of Biochemistry, University of Nijmegen, The Netherlands.

Permeabilized rabbit pancreatic acinar cells were used to study the effects of Ca2+ pump inhibition and Ca2+ store depletion on the sensitivity of internal Ca2+ stores to emptying by inositol 1,4,5- trisphosphate (Ins-1,4,5-P3). Complete inhibition of pump activity by thapsigargin resulted in the monoexponential loss of 92% of the actively stored Ca2+ with a half-time of 6.2 min. Under these conditions, Ca2+ release evoked by a submaximal concentration of Ins- 1,4,5-P3 did not cease after 1.5 min, as was observed in the absence of thapsigargin, but continued for at least 5 min. This observation suggests that under normal conditions of Ca2+ pumping, a substantial part of the internal Ca2+ stores is not depleted by the action of Ins- 1,4,5-P3 due to compensatory Ca2+ uptake. Evidence in support of the idea of compensatory Ca2+ pumping was obtained in exchange experiments performed in the absence of thapsigargin. The slow kinetics of sustained Ca2+ release in the absence of Ca2+ pump activity suggests that Ca2+ is released from stores containing either relatively few or less sensitive Ins-1,4,5-P3-operated Ca2+ release channels. Gradual emptying of the internal Ca2+ stores by thapsigargin did not affect the potency with which Ins-1,4,5-P3 released Ca2+, indicating that the intravesicular Ca2+ content does not control the sensitivity of the Ins- 1,4,5-P3-operated Ca2+ channel to activation by Ins-1,4,5-P3. This was confirmed using ruthenium red, which preferentially depleted the Ins- 1,4,5-P3-releasable store without affecting the EC50 for Ins-1,4,5-P3- stimulated Ca2+ release. The data presented indicate that the quantal type of Ca2+ release observed with Ins-1,4,5-P3 requires compensatory Ca2+ pumping. Moreover, they support the idea that internal Ca2+ stores display differential sensitivities toward Ins-1,4,5-P3 rather than responding uniformly to this internal Ca(2+)-mobilizing messenger.
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