Dissociation between stimulant-evoked acinar membrane resistance change and amylase secretion in the mouse parotid gland.

1. Isolated segments of mouse parotid gland were superfused with a physiological saline solution. Membrane potential and input resistance were measured with intracellular micro-electrodes. Amylase secretion was monitored using an automated fluorometric assay. The parotid gland was stimulated by exposure to isoprenaline (10(-6)M), ACh (10(-6) M), dibutyryl or monobutyryl cyclic AMP (10(-3)M). 2. ACh evoked a sharp decrease in input resistance (from about 3-6 M omega to 1-2 M omega ) accompanied by a modest (two-fold) increase in amylase output. Both effects were fully reversible. 3. Isoprenaline evoked a marked increase in amylase output (five to ten-fold) reaching maximum after 20-30 min of stimulation. Throughout the period of intensive secretion the input resistance remained at the control level. Short pulses of ACh stimulation dramatically reduced input resistance in this period. 4. Dibutyryl cyclic AMP and monobutyryl cyclic AMP caused marked increases in amylase output (five to ten-fold) peaking 40-50 min after start of the continuous stimulation. This increase in amylase secretion was not accompanied by any change in input resistance. Short pulses of ACh stimulation sharply and reversibly reduced input resistance both in control and test periods. 5. It is concluded that the ACh-evoked reduction in input resistance is not a consequence of the secretory event and that secretion does not itself cause a decrease in input resistance.