Does basal cholinergic activity potentiate exogenous secretin for stimulation of pancreatic bicarbonate output in dogs?

In conscious dogs with gastric and pancreatic Thomas fistulas, we studied the effect of atropine sulfate (20 micrograms kg-1 h-1 intravenously) on bicarbonate output basally and in response to intravenous infusion of synthetic secretin (62.5, 125, 250, 500, 1,000 and 2,000 ng kg-1 h-1). We analyzed the data in an attempt to determine whether basal cholinergic activity potentiates the pancreatic bicarbonate response to secretin. Assuming that atropine suppresses all basal cholinergic activity, C (= bicarbonate response to basal cholinergic activity alone) was calculated by subtracting basal pancreatic bicarbonate output with atropine from that without atropine, S (= response to secretin alone) was calculated by subtracting basal pancreatic bicarbonate output with atropine from that in response to secretin with atropine. SwC was defined as the response to secretin acting simultaneously with (w) basal cholinergic activity and was calculated by subtracting basal pancreatic bicarbonate output with atropine from the response to secretin without atropine. If SwC was significantly greater than S + C (= sum of effects of stimulus alone and basal cholinergic activity alone) potentiation between basal cholinergic activity and secretin was assumed to exist. C was 30 +/- 9 mumol 15 min-1 for bicarbonate output. SwC of bicarbonate output was significantly (p less than 0.05) greater than S + C in response to the four lowest doses (62.5-500 ng kg-1 h-1) of secretin. We conclude that potentiation exists between basal cholinergic activity and low doses of exogenous secretin. Thus, basal cholinergic activity is an important modulator of pancreatic bicarbonate response to secretin.