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Journal of Dental Research, Vol 67, 561-564, Copyright © 1988 by International & American Associations for Dental Research Online Journals
ARTICLES |
J. R. Martinez and P. Reed
Department of Child Health, University of Missouri School of Medicine, Columbia 65212.
Dispersed salivary acini isolated from the rat submandibular gland by enzymatic digestion were used to study the effects of alpha-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 mumol/L) alone did not modify 36Cl accumulation but in the presence of the beta-receptor blocker propranolol (1 mumol/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 mumol/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 alpha-agonist phenylephrine (10 mumol/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 alpha-receptor blocker phentolamine, or the beta-agonist isoproterenol, increased the tracer content of the cells, whether the drugs were added at time zero or to tracer-pre-loaded cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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