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Secretagogues at concentrations greater than those required for maximum secretory responses (as measured in pancreatic protein output and juice flow) induce submaximal responses. In the isolated perfused rat pancreas, a high concentration ofcholecystokininoctapeptide (1 or 100 nM CCK-8) produced secretory responses significantly smaller than maximal responses. This hyporeactive response to supraoptimal stimulation coincided with a profound alteration in acinar cell morphology as follows: 1) disappearance of microvilli from the luminal acinar cell surface, 2) appearance of cytoplasmic ‘lakes’ of zymogen material bounded by a membrane and located among normal looking mitochondria and cisternae of granular endoplasmic reticulum, and 3) destruction of cytoplasmic microfilaments detected immunohistochemically by an anti-actin antibody. In contrast to these alterations, stimulation with 1 nM CCK-8 in combination with 100 pM secretin: 1) preserved the acinar cell ultrastructure and microfilaments so that they resembled those in the control pancreas (without stimulation) and pancreas stimulated with lower doses of CCK-8; and 2) regained the maximal secretory responses equivalent to those with the optimal CCK-8 concentration of 100 pM. It is concluded, therefore, that: 1) secretin prevents the hyporeactive and morphological alteration of pancreatic acinar cell induced by supraoptimal stimulation with CCK-8; and 2) the alterations may be mediated by microfilaments containing immunoreactive actin. These observations provide an experimental basis for the administration of secretin to prevent the development of pancreatitis induced by a supraoptimal plasma CCK level. Functionally, the exocrine pancreas consists of vagus nerve, vasoactive intestinal polypeptide acinar tissue and ductal tissue. Stimulus-secretion coupling in the acinar cells is initiated by the activation of a receptor for the peptide hormone, cholecystokinin-pancreozymin (CCK), as well as by the activation of a muscarinic cholinergic receptor (4, 36). Pancreatic juice secretion by the ductal cells is regulated by another peptide hormone, secretin, and a neurotransmitter of the (VIP) (8). Studies in recent years have developed the view that, on the acinar cell, not only CCK and cholinergic receptors but also secretin and VIP receptors are present (10). Interactions among the intracellular processes followed by the activation of these receptors have also been studied. Stimulation of the acinar tissue with various

biomedical research

&lt;b&gt;SECRETIN PREVENTS HYPOREACTIVE AND MORPHOLOGICAL RESPONSES OF RAT PANCREATIC ACINAR CELLS TO STIMULATION WITH SUPRAOPTIMAL CONCENTRATION OF &lt;/b&gt;&lt;b&gt;CHOLECYSTOKININ-OCTAPEPTIDE &lt;/b&gt;