Answers are grounded in this paper and cite their sources.
Effect of neuroactive agents on cholecystokinin release from the isolated, perfused porcine duodenum. Acta Physiol Scand130, 627–632. Received 26 April 1986, accepted 8 March 1987, ISSN 0001–6772. Departments of Clinical Chemistry and Surgery C, Rigshospitalet, and Institute of Medical Physiology C, The Panum Institute, University of Copenhagen, Denmark. To elucidate the mechanisms involved in the regulation of CCK release from the small intestine, the effect of neuroactive agents on the release of CCK from the isolated, perfused porcine duodenum has been studied. CCK in the venous effluent was measured by three radio‐immunoassays specific for the N‐terminus, the tyrosin‐o‐sulphated region and the C‐terminus of CCK‐33. Gastrin‐releasing peptide (GRP) at concentrations of 10‐‐10 and 10‐‐9 M in the arterial line increased the CCK output by about 100 and 500%, respectively, as measured with the assay specific for the sulphated region of CCK. Pilocarpine and physostigmine at concentrations of 10‐‐5 m reduced the CCK output to 24 and 40% of basal, respectively, and also abolised the GRP‐stimulated CCK response. Atropine (10‐‐6 M) increased CCK output about 100%. The results suggest that both stimulatory and inhibitory nervous impulses may be transmitted to the intestinal CCK cell, mediated by intramural GRP neurons and cholinergic pathways, respectively.
No takes yet. Share an insight, caveat, or question.
Cantor et al. (1987) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: