Nov 1, 1986

Defective beta-adrenergic secretory responses in submandibular acinar cells from cystic fibrosis patients

M A McPhersonM C Goodchild


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.

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  • Citations37


Mentioned in this Paper

Metabolic Process, Cellular
Mucin-1 protein
Cyclic AMP
Cystic Fibrosis
Thyroid Hormone Plasma Membrane Transport Defect
Norepinephrine, (+, -)-Isomer
Process of Secretion
Amylase Measurement
Metabolic Pathway

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