The microfilaments in the acinar cell of the exocrine pancreas are essentially located in the apical part of the cell: thin microfilaments (50 A), cytochalasin B (CB)-sensitive, form the axis of the microvilli and a network lying beneath the apical membrane; thicker filaments (100 A), at least partly CB-insensitive, form bundles parallel to the plasma cell membrane and the desmosomal links. CB interaction with the acinar cell of the exocrine pancreas involves at least two sites: a membrane site involved in the inhibitory effect of CB on the monosaccharide transport and a less sensitive site at the filamentous level at least partly responsible for the inhibitory effect of CB in the secretion of the exportable enzyme from the pancreatic cell. CB did not alter the energy balance of the acinar cell nor the exchanges of 45Ca between the extracellular medium and the pancreatic tissue. CB (2 x 10 -7 and 2 x 10 -6 M) has secretagogue properties whereas CB (2 • 10 -s M) has inhibitory effect on stimulated secretion and secretagogue properties. The mechanism of these secretory effects is not yet explained. The analysis presented in this investigation affords strong evidence for the involvement of the microfilamentous network in the last steps of the secretory cycle in the acinar cell of the exocrine pancreas.
DbcAMP greater than or equal to 0.1 mM induces the discharge of exportable enzymes from rat pancreas fragments incubated in vitro. This effect is qualitatively similar to the action of physiological secretagogues acting via hormone receptors: 1) it is accompanied by the appearance of exocytotic images at the acinar cell apex; 2) it is energy dependent but energy supply is low while that required for the carbamylcholine or caerulein response is high and can only be afforded by oxidative phosphorylation; 3) it is calcium dependent, but no alteration of inward or outward calcium movement can be observed; 4) it is altered by agents known to disrupt the microfilamentous microtubular system [41]. However, the secretory response to DbcAMP is quantitatively less than that obtained with hormonal stimuli. A damaging effect of DbcAMP on pancreatic acinar cells is ruled out on histological and biochemical grounds: there is no significant leakage of LDH; protein synthesis, 2-deoxy-D-glucose and L-leucine uptake are unaltered. The secretagogue effect of DbcAMP is reversible, dose-related and specific. It is not mediated by neurotransmitter release or by interaction with their receptors. The evidence presented points to a direct interaction of DbcAMP on the pancreatic acinar cell and suggests the last step of the secretory cycle as the most probable site of action of the nucleotide derivative.
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