| Abstract: | Dispersed acini from dog pancreas were used to examine the ability of dopamine to increase cyclic AMP cellular content and the binding of 3H]dopamine. Cyclic AMP accumulation caused by dopamine was detected at 1·10−8 M and was half-maximal at 7.9±3.4·10−7M. The increase at 1·10−5 M, (7.5-fold) was equal to the half-maximal increase caused by secretin at 1·10−9 M. Haloperidol, a dopaminergic receptor antagonist inhibited cyclic AMP accumulation caused by dopamine. The IC50 value for haloperidol, calculated from the inhibition of cyclic AMP increase caused by 1·10−5 M dopamine was 2.3±0.9·10−6M. Haloperidol did not alter basal or secretin-stimulated cyclic AMP content. 3H]Dopamine binding was studied on the same batch of cells as cyclic AMP accumulation. At 37°C, it was rapid, reversible, saturable and stereospecific. The Kd value for high affinity binding sites was 0.43±0.1·10−7M and 4.7±1.6·10−7M for low affinity binding sites. The concentration of drugs necessary to inhibit specific binding of dopamine by 50% was 1.2±0.4·10/t-7M noradrenaline, 2·10/t-7 M epinine, 4.1±1.8·10/t-6M fluphenazine, 8.0±1.6·10/t-6M haloperidol, 4.2±1.2·10−6Mcis-flupenthixol, 2.7±0.4·10−5Mtrans-flupenthixol, >1·10−5M apomorphine, sulpiride, naloxone and isoproterenol. |
