Key result
Carbachol increased the rate of 45Ca efflux and alpha-amylase secretion from rat pancreas tissue, an effect blocked by atropine, suggesting intracellular calcium sustains stimulus-secretion coupling.
Intracellular calcium can sustain stimulus-secretion coupling in the rat exocrine pancreas.
Animal data implicate intracellular calcium in rat pancreatic secretion; hypothesis-generating and should not yet inform clinical practice.
1 The efflux of (45)Ca from rat pancreas was investigated in relation to the secretion of alpha-amylase.2 The (45)Ca space in the pancreas was increased 1.6 times when pancreatic tissue was incubated in media in which the extracellular calcium concentration was reduced from 1.0 to 0.05 mM.3 Carbachol increased the rate of (45)Ca efflux from the tissue and this effect was associated with an increase in the release of alpha-amylase. Dibutyryl cyclic adenosine monophosphate (AMP) also evoked a secretory response, but did not alter the rate of (45)Ca efflux. In combination with carbachol, the dibutyryl analogue of cyclic AMP reduced the carbachol-stimulated increase in (45)Ca efflux while enhancing the release of secretory protein.4 The stimulatory effect of carbachol on (45)Ca efflux was observed when pancreatic tissues were incubated in media containing a high concentration of ethyleneglycolbis (beta-aminoethyl)-N,N'-tetraacetic acid (EGTA).5 Atropine blocked the effects of carbachol on both (45)Ca efflux and secretion of alpha-amylase.6 It was concluded that intracellular calcium can and may sustain stimulus-secretion coupling in the rat exocrine pancreas.
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S. Heisler (1974) studied this question. Carbachol was evaluated on Calcium efflux and secretion of alpha-amylase. Carbachol increased the rate of 45Ca efflux and alpha-amylase secretion from rat pancreas tissue, an effect blocked by atropine, suggesting intracellular calcium sustains stimulus-secretion coupling.
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