Abstract
We studied chloride efflux from isolated rabbit pancreatic acini in suspension, by loading with 36Cl to steady state and rapidly washing acini by filtration to determine 36Cl cpm/micrograms DNA remaining. Linear loss of acinar chloride occurred over 5 min (k = 0.038 +/- 0.008 min-1, n = 5). Forskolin (5 x 10(-5) M) increased the rate of chloride efflux (k = 0.100 +/- 0.016 min-1, n = 5, p less than 0.001) 2.6-fold. At 5 min, forskolin increased acinar cAMP levels (1065 +/- 254 versus 7 +/- 2 pmol/mL, n = 5, p less than 0.005) and percentage of chloride efflux (37.4 +/- 2.3 versus 26.0 +/- 2.2%, n = 13, p less than 0.005). The chloride channel inhibitor anthracene-9-carboxylic acid (10(-3) M) had no effect on chloride loss from acini exposed to vehicle (30.9 +/- 1.9 versus 29.9 +/- 2.3%, n = 4), but completely inhibited forskolin-stimulated efflux at 5 min (40.0 +/- 2.4 versus 29.3 +/- 2.4%, n = 5, p less than 0.005). Manipulation of extracellular calcium concentration demonstrated that chloride efflux was not coupled to zymogen granule amylase release. Secretin (10(-7) M) increased acinar cAMP levels (68 +/- 22 versus 7 +/- 2 pmol/mL, n = 5, p less than 0.05) and significantly increased the loss of chloride from acini (34.9 +/- 1.4 versus 26.1 +/- 1.7%, n = 7, p less than 0.005) without affecting amylase release. Secretagogue-stimulated amylase release by cholecystokinin octapeptide (10(-8) M) and carbamylcholine (10(-5) M), did not increase chloride efflux at 5 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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