title: Functional characteristics of atrophic parotid acinar cells from rats after liquid feeding.
abstract: Rat parotid atrophy, induced by liquid feeding over 10 days, was manifested as gland weight loss (40%) and histologically as acinar shrinkage. Acinar secretory function was investigated in the same glands using enzymatically dispersed cell preparations and superfused gland slices. Results were normalized for the acinar proportional volume, determined by stereological analysis. Although total amylase activity was significantly lower in liquid-fed (LD) rats, the percentage amylase releases elicited by isoproterenol (10 mumol/L) and carbachol (10 mumol/L) were unchanged from controls (CON). Superfused gland slices from LD and control (CON) rats exhibited increases in membrane permeability (86Rb+ efflux) and in the efflux and re-uptake of K+ in response to acetylcholine (10 mumol/L). However, the recorded maxima were significantly lower in LD than in CON (86Rb+, 27% lower; K+ efflux, 35% lower; K+ re-uptake, 35% lower). Similarly, after 60-minute equilibration, the 36Cl- content of cells from LD rats was 57% lower than that from CON. Carbachol (10 mumol/L), acting for 1 min with bumetanide (100 mumol/L), elicited an efflux of 36Cl- from cells from LD rats, but this was significantly lower (32.2%) in LD than in CON (49.9%). The reduced levels of ion movement are probably commensurate with the reduced acinar cell volume occurring in LD rats. These results show that mechanisms for the formation of primary saliva (exocytosis and transepithelial ion movements) are substantially preserved in the altered acinar cells of LD rats. Thus, in salivary disorders, severe morphological acinar atrophy may not inevitably signify exhausted secretory function.
authors.affiliation: Salivary Research Group, Liverpool University Dental Hospital and School of Dentistry, United Kingdom.
authors.forename: J
authors.initials: J
authors.lastname: Scott
authors.forename: D L
authors.initials: DL
authors.lastname: Gunn
mesh_terms: D000681:Amylases / Q000378:metabolism; D000818:Animals; D001284:Atrophy; D002712:Chlorides / Q000378:metabolism; D004195:Disease Models, Animal; D005089:Exocytosis; D005526:Food, Formulated / Q000009:adverse effects*; D017136:Ion Transport; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009929:Organ Size; D010305:Parotid Diseases / Q000209:etiology / Q000503:physiopathology*; D010306:Parotid Gland / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D011976:Receptors, Muscarinic / Q000187:drug effects; D012463:Saliva / Q000378:metabolism*
chemical_list: D002712:Chlorides; D011976:Receptors, Muscarinic; D000681:Amylases; D007545:Isoproterenol