We propose that L-DOPA by itself is a neurotransmitter. Recently, we identified G-protein coupled receptor (GPCR) GPR143, a gene product of ocular albinism-1, as a receptor for L-DOPA. During the course of our study, we found that the pressor response to adrenergic receptor alpha1 (ADRA1) agonist phenylephrine was attenuated in GPR143 gene-deficient mice (Gpr143^-/y) when compared with wild type (WT) mice. Phenylephrine increased ERK phosphorylation in the ADRA1B expressing HEK293T cells. The phenylephrine-induced increase in ERK phosphorylation was augmented by coexpression of GPR143 and ADRA1B. Co-immunoprecipitation analysis revealed that GPR143 interacted with ADRA1B. To identify whether the augmentation by GPR143 was due to interaction between GPR143 and ADRA1, we screened some compounds that suppress the hetero-oligomerization using ERK phosphorylation and co-immunoprecipitation assays. Compound A (1 μM) attenuated both augmentation by GPR143 of phenylephrine-induced ERK phosphorylation and the interaction between GPR143 and ADRA1B. These results suggest that GPR143 augments the ADRA1B-mediated response via hetero-oligomerization between GPR143 and ADRA1B.