Effect of alpha-receptor stimulation on Cl transport by rat submandibular acini.

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)