Effect of a-Receptor Stimulation on Cl Transport by Rat Submandibular Acini
- 1 March 1988
- journal article
- research article
- Published by SAGE Publications in Journal of Dental Research
- Vol. 67 (3) , 561-564
- https://doi.org/10.1177/00220345880670030701
Abstract
Dispersed salivary acini isolated from the rat submandibular gland by enzymatic digestion were used to study the effects of a-receptor stimulation on transmembrane transport of 36Cl. In the absence of secretagogue, the tracer accumulated in the cells in a time-dependent manner until a steady-state content of 6.8 ± 0.1 nmol/mg protein was attained after 3-5 min of incubation. Epinephrine (1 μmol/L) alone did not modify 36Cl accumulation but in the presence of the β-receptor blocker propranolol (1 μmol/L) caused a significant (21%) reduction in the isotope content of the cells to 5.2 ± 0.1 nmol/mg protein. In acini pre-loaded with 36Cl for 12 min, 1 μmol/L epinephrine caused a rapid but transient net efflux of tracer, but the isotope content subsequently increased to pre-stimulation levels. In the presence of propranolol, however, the efflux of 36Cl induced by epinephrine was larger and more sustained and was partially inhibited by the K-channel blocker quinidine (1 mmol/L) and significantly by the absence of Ca2+ in the incubation medium. The a-agonist phenylephrine (10 μmol/L) also significantly reduced the steady-state 36Cl content of tracer-pre-loaded cells. By contrast, exposure of the acini to epinephrine in the presence of the a-receptor blocker phentolamine, or the β-agonist isoproterenol, increased the tracer content of the cells, whether the drugs were added at time zero or to tracer-pre-loaded cells. The results indicate that stimulation of a-receptors in salivary acinar cells causes a Ca2+-dependent efflux of Cl which seems to be functionally linked to K release. These effects are similar to those observed following stimulation of cholinergic receptors. The lack of effect of β-receptor stimulation on Cl efflux suggests that this response is not regulated by a cAMP-mediated pathway in salivary cells. The extent of stimulation-induced Cl efflux is likely to be relevant in terms of the amount of saliva secreted upon stimulation.This publication has 16 references indexed in Scilit:
- Abnormal 45Ca Fluxes in Dispersed Submandibular Acini of Rats Treated with ReserpineJournal of Dental Research, 1987
- An examination of functional linkage between K efflux and 36Cl efflux in rat submandibular salivary gland acini in vitroArchives of Oral Biology, 1987
- 36Cl fluxes in dispersed rat submandibular acini: Effects of Ca2+ omission and of the ionophore A23187Pflügers Archiv - European Journal of Physiology, 1986
- Identification of Cellular Activation Mechanisms Associated with Salivary SecretionAnnual Review of Physiology, 1986
- Adrenergic regulation of ion transport by primary cultures of canine tracheal epithelium: Cellular electrophysiologyThe Journal of Membrane Biology, 1986
- Cl?-channels in the apical cell membrane of the rectal gland ?induced? by cAMPPflügers Archiv - European Journal of Physiology, 1985
- 36Cl fluxes in dispersed rat submandibular acini: Effects of acetylcholine and transport inhibitorsPflügers Archiv - European Journal of Physiology, 1985
- Basic Biological Sciences Regulation of Tight Junctional Permeability in the Rat Parotid Gland by Autonomic AgonistsJournal of Dental Research, 1984
- THE EFFECT OF PHENYLEPHRINE ON EXCRETION OF FLUID AND ELECTROLYTES BY THE PAROTID AND MANDIBULAR GLANDS OF THE RATImmunology & Cell Biology, 1979
- Calcium ion uptake induced by cholinergic and ?-adrenergic stimulation in isolated cells of rat salivary glandsPflügers Archiv - European Journal of Physiology, 1977