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Effect of a-Receptor Stimulation on Cl Transport by Rat Submandibular Acini

Department of Child Health, University of Missouri School of Medicine, Columbia, Missouri 65212

P. Reed

Department of Child Health, University of Missouri School of Medicine, Columbia, Missouri 65212

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.

Journal of Dental Research, Vol. 67, No. 3, 561-564 (1988)
DOI: 10.1177/00220345880670030701


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