{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T00:28:02Z","timestamp":1771633682729,"version":"3.50.1"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1984,11,1]],"date-time":"1984-11-01T00:00:00Z","timestamp":468115200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1984,11]]},"abstract":"<jats:p>The technique of electrical field stimulation (e.f.s.) was employed in conjunction with selective pharmacological antagonists to specifically investigate the role of endogenous neurotransmitter(s) in the activation of beta\u2010adrenergic receptor mechanisms in isolated parotid gland segments of the rat. The field\u2010stimulus\u2010induced amylase release due to beta\u2010adrenergic receptor activation was characterized as that persisting in the presence of atropine (10(\u20105) M) and phentolamine (10(\u20105) M) and susceptible to blockade by propranolol (5 X 10(\u20106) M), i.e. combined beta 1\u2010 and beta 2\u2010receptor blockade. The selective beta 1\u2010receptor antagonist metoprolol (10(\u20105) M) was as effective as propranolol in blocking the beta\u2010mediated enzyme release. The selective beta 2\u2010receptor antagonist, H35\/25 (10(\u20105) M) did not significantly affect the field\u2010stimulus\u2010induced amylase release. In the absence of any phosphodiesterase inhibitor the levels of cyclic AMP in the tissues were close to the limit of detection. Field stimulation was however associated with a fourfold increase in cyclic AMP. By comparison isoprenaline (10(\u20105) M) gave rise to a tenfold increase in cyclic AMP. The changes in cyclic AMP metabolism, in response to both field stimulation and isoprenaline, were greatly enhanced in the presence of the phosphodiesterase inhibitor 3\u2010isobutyl\u20101\u2010methylxanthine (IBMX). The field\u2010stimulus\u2010induced increase in cyclic AMP was abolished by the beta 1\u2010adrenergic receptor antagonist, metoprolol, but persisted in the presence of the beta 2\u2010adrenergic antagonist, H35\/25. IBMX was found to have a potent direct effect on amylase release. IBMX (10(\u20103) M) also gave rise to a tenfold increase in cyclic AMP. IBMX is then as effective as 10(\u20105) M\u2010isoprenaline in stimulating both enzyme secretion and cyclic AMP metabolism. The secretory response to IBMX was unaffected by beta\u2010adrenergic blockade by propranolol, was independent of extracellular calcium and did not give rise to 86Rb+ efflux. Importantly, isoprenaline (10(\u20105) M) failed to evoke any significant increase in amylase release if introduced during sustained superfusion of IBMX, yet it is in such protocols that the greatest changes in cyclic AMP metabolism are seen. The study clearly demonstrates that the beta\u2010adrenergic\u2010receptor\u2010regulated amylase release in response to nerve stimulation is mediated predominantly, if not exclusively, by the beta 1\u2010receptor subtype.(ABSTRACT TRUNCATED AT 400 WORDS)<\/jats:p>","DOI":"10.1113\/jphysiol.1984.sp015468","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T06:47:57Z","timestamp":1418971677000},"page":"335-348","source":"Crossref","is-referenced-by-count":13,"title":["Beta\u2010adrenergic receptor mechanisms in rat parotid glands: activation by nerve stimulation and 3\u2010isobutyl\u20101\u2010methylxanthine."],"prefix":"10.1113","volume":"356","author":[{"given":"C M","family":"Fuller","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D V","family":"Gallacher","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1984,11]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1984.sp015468","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1984.sp015468","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,21]],"date-time":"2023-10-21T00:36:03Z","timestamp":1697848563000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1984.sp015468"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1984,11]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1984,11]]}},"alternative-id":["10.1113\/jphysiol.1984.sp015468"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1984.sp015468","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1984,11]]}}}