Abstract
Anion replacement experiments were performed on superfused in vitro mouse pancreatic tissue and the effects on the electrical response of acinar cells to ACh [acetylcholine] investigated. Electrical measurements were made with 2 micro-electrodes inserted into electrically coupled cells. ACh was applied by microionophoresis. Potential recordings were taken before, during and after changeover from the control superfusion fluid, containing Cl-, to one containing the substituted anion. The tested anions were classified into 3 groups: Cl--like anions Br-, I- and NO3- (group I), causing no change or a negative displacement of the ACh null-potential, compared to that measured in the control Cl- containing solution and only small changes in the resting and stimulated electrical properties of the acinar cell; ions less permeable than Cl-: isethionate, acetate, sulfate and hippurate (group II), showing a positive displacement of the ACh null-potential and a similar or increased resting cell input resistance; and methylsulfate and benzenesulfonate (group III), causing a negatively displaced ACh null-potential but showing changes in the resting electrical properties of the acinar cells characteristic of anions in group II. The ACh null-potential sequence, in order of decreasing negativity, was NO3- .gtoreq. benzenesulfonate .gtoreq. I- .gtoreq. methylsulfate > Br- .gtoreq. Cl- > isethionate > acetate .gtoreq. sulfate > hippurate. Experiments involving the use of bicarbonate demonstrated that it apparently does not contribute significantly to the value of the ACh null-potential. The sequence of the anions in group I were compared to the Eisenman series I, suggesting the ACh-opened Cl- pathway probably comprises a large hydrated ion channel bearing a lining of weak positive charges. A quantitative relationship was sought between the ACh null-potential and extracellular Cl-. A 10-fold reduction in the extracellular concentration apparently resulted in a 15 mV positive shift of the null-potential.