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THE EFFECT OF DIBUTYRYL CYCLIC ADENOSINE‐3′,5′‐MONOPHOSPHATE ON PROTEIN SECRETION FROM THE RAT EXOCRINE PANCREAS in vitro
Author(s) -
FAST D.,
TENENHOUSE A.
Publication year - 1976
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1976.tb08630.x
Subject(s) - carbachol , endocrinology , medicine , adenosine , extracellular , intracellular , calcium , biology , cyclic adenosine monophosphate , chemistry , secretion , stimulation , biochemistry , receptor
1 The mechanism by which dibutyryl cyclic adenosine‐3′‐5′‐monophosphate (dibutyryl cyclic AMP) potentiates the secretory effect of carbachol in rat exocrine pancreas was investigated. 2 Dibutyryl cyclic AMP potentiated the secretory effect of carbachol only at carbachol concentrations ⋝10 −7 mol/l; was independent of carbachol at concentrations > 10 −7 mol/l and was inversely proportional to extracellular [Ca 2+ ]. 3 Carbachol increased and dibutyryl cyclic AMP reduced the rate of 45 Ca efflux from the tissue. 4 A‐23187 stimulated 3 H‐protein release in the presence of Ca 2+ and this effect was potentiated by dibutyryl cyclic AMP; the degree of potentiation was inversely proportional to extracellular [Ca 2+ ]. At 10 −3 mol/l [Ca 2+ ] the potentiation occurred only at ionophore concentrations ⋜ 10 −6 mol/litre. 5 These results support the hypothesis that dibutyryl cyclic AMP potentiates the effect of secretagogues in rat exocrine pancreas by maintaining an elevated intracellular calcium concentraion. It does so by inhibiting Ca 2+ efflux. The results also suggest that the limiting factor in carbachol‐stimulated secretion, at all concentrations of carbachol, is intracellular [Ca 2+ ].