Defective beta-adrenergic secretory responses in submandibular acinar cells from cystic fibrosis patients.
The in-vitro investigation of secretory responses of submandibular tissues from three cystic fibrosis (CF) patients and four control subjects showed that responses to a beta-adrenergic stimulus (isoproterenol) were much poorer in CF cells than in control cells. The beta-adrenergic secretory responses of the CF cells (as measured by amylase and mucin secretion) were increased in the presence of 3-isobutyl-l-methyl xanthine, a cyclic nucleotide phosphodiesterase inhibitor. Perhaps an alteration in a regulator of cyclic adenosine monophosphate and Ca2+ metabolism in CF cells is responsible for the decrease in beta-adrenergic function. This proposal would account for the defective regulation of protein secretion, Cl- transport, and Ca2+ homoeostasis in CF exocrine cells and thus might be directly related to the genetic defect.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000328:Adult; D000681:Amylases / Q000378:metabolism; D002478:Cells, Cultured; D002648:Child; D003550:Cystic Fibrosis / Q000503:physiopathology*; D006801:Humans; D007223:Infant; D007545:Isoproterenol / Q000494:pharmacology; D008875:Middle Aged; D009077:Mucins / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D013363:Submandibular Gland / Q000187:drug effects / Q000378:metabolism*; D013566:Sympathomimetics / Q000494:pharmacology*
D009077:Mucins; D013566:Sympathomimetics; D000681:Amylases; D007545:Isoproterenol; D015056:1-Methyl-3-isobutylxanthine; D009638:Norepinephrine