{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T00:08:17Z","timestamp":1768781297143,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[1996,2,1]]},"abstract":"<jats:p> Previously, it has been shown that an increase in adenosine 3',5'-cyclic monophosphate (cAMP) levels stimulates intestinal secretion of cholecystokinin (CCK); however, the mechanisms for increasing intracellular cAMP levels are not known. Using the CCK-secreting intestinal cell line, STC-1, we evaluated whether beta-adrenergic receptors (beta-ARs) might be present on STC-1 cells and whether they stimulated CCK release through increases in cAMP. Photoaffinity labeling of beta-ARs from solubilized STC-1 cell membranes revealed photoincorporation of the agonist [125I]iodocyanopindolol into an approximately 75-kDa band. Addition of the beta-AR agonist, isoproterenol, in the presence of 3-isobutyl-1-methylxanthine, produced a concentration-dependent increase in both cAMP levels and CCK release. Blockade of beta 1- and\/or beta 2-ARs significantly inhibited isoproterenol-stimulated increases in cAMP production and CCK release. With the use of fura 2-loaded cells to measure changes in intracellular Ca2+ concentration ([Ca2+]i), isoproterenol stimulation was found to increase cytosolic Ca2+ levels. To evaluate whether this increase in [Ca2+]i was due to release of Ca2+ or influx of Ca2+, cells were treated with the L-type calcium channel blocker, diltiazem, which inhibited isoproterenol-stimulated CCK secretion. Furthermore, in patch-clamp studies with inside-out membrane patches, addition of the catalytic subunit of protein kinase A activated diltiazem-sensitive Ca2+ channels. It is concluded that beta-ARs are present on STC-1 cells and are coupled to the production of cAMP, which may increase CCK release through a calcium-dependent process. <\/jats:p>","DOI":"10.1152\/ajpgi.1996.270.2.g291","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T05:59:29Z","timestamp":1514095169000},"page":"G291-G297","source":"Crossref","is-referenced-by-count":6,"title":["Beta-adrenergic regulation of cholecystokinin secretion in STC-1 cells"],"prefix":"10.1152","volume":"270","author":[{"given":"L.","family":"Scott","sequence":"first","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, NorthCarolina 27710, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"V.","family":"Prpic","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, NorthCarolina 27710, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W. D.","family":"Capel","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, NorthCarolina 27710, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Basavappa","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, NorthCarolina 27710, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. W.","family":"Mangel","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, NorthCarolina 27710, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T. W.","family":"Gettys","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, NorthCarolina 27710, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. A.","family":"Liddle","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, NorthCarolina 27710, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajpgi.1996.270.2.G291","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:11:56Z","timestamp":1567973516000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajpgi.1996.270.2.G291"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1996,2,1]]}},"alternative-id":["10.1152\/ajpgi.1996.270.2.G291"],"URL":"https:\/\/doi.org\/10.1152\/ajpgi.1996.270.2.g291","relation":{},"ISSN":["0193-1857","1522-1547"],"issn-type":[{"value":"0193-1857","type":"print"},{"value":"1522-1547","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,2,1]]}}}