The aim of this study was to investigate the role of the K+ conductance in unstimulated and stimulated pancreatic ducts and to see how it is affected by provision of exogenous HCO3-/CO2. For this purpose we have applied electrophysiological techniques to perfused pancreatic ducts, which were dissected from rat pancreas. The basolateral membrane potential PDbl of unstimulated duct cells was between -60 mV and -70 mV, and the cells had a relatively large K+ conductance in the basolateral membrane as demonstrated by (a) 20-22 mV depolarization of PDbl in response to increase in bath K+ concentration from 5 mmol/l to 20 mmol/l and (b) the effect of a K+ channel blocker, Ba2+ (5 mmol/l), which depolarized PDbl by 30-40 mV. These effects on unstimulated ducts were relatively independent of bath HCO3-/CO2. The luminal membrane seemed to have no significant K+ conductance. Upon stimulation with secretin or dibutyryl cyclic AMP, PDbl depolarized to about -35 mV in the presence of HCO3-/CO2. Notably, the K+ conductance in the stimulated ducts was now only apparent in the presence of exogenous HCO3-/CO2 in the bath solutions. Upon addition of Ba2+, PDbl depolarized by 13 +/- 1 mV (n = 7), the fractional resistance of the basolateral membrane, FRbl increased from 0.66 to 0.78 (n = 6), the specific transepithelial resistance, Rte, increased from 52 +/- 13 omega cm2 to 59 +/- 15 omega cm2 (n = 11), and the whole-cell input resistance, Rc, measured with double-barrelled electrodes, increased from 20 M omega to 26 M omega (n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)