The beta(1)-adrenergic receptor (beta(1)AR) gene contains binding sites for myc/max proteins within a glucocorticoid response element. Transcriptional activation of the beta(1)AR is the result of cooperative binding between c-myc and the glucocorticoid receptor on the beta(1)AR promoter. The transcriptional regulation of both beta(1)AR and c-myc are developmentally regulated. We used transcription rate assays of nuclei isolated from fetal hearts to demonstrate a fivefold increase in the transcription rate of beta(1)AR vs. postnatal hearts (P < 0.01). This was associated with a fourfold increase in c-myc transcription. Transcription rate assays performed in a rat fibroblast cell line that overexpresses c-myc (myc(+/+)) showed similarly increased beta(1)AR expression compared with the wild-type cell line. Transient transfection experiments in the myc(+/+) cells demonstrated robust expression of beta(1)AR promoter constructs, which was abrogated by mutation of the myc/max binding site or by cotransfection with a c-myc antisense expression vector. These results suggest that the regulation of cardiac beta(1)AR transcription and the expression of c-myc are tightly integrated.