The promoter of the human atrial light chain (hALC-1) contains two transcriptional start sites, a proximal and a distal. To analyse their functional importance, we generated stably transfected H9c2 cardiomyoblasts either with the full length promoter or a deleted promoter. We demonstrated that the deleted promoter and the full length promoter have equal basal activities. However, both transcriptional start sites are required for vasopressin (5mM) stimulation (p < 0.001). The treatment with estrogen (5mM) and testosterone (5mM) alone did not influence the hALC-1 promoter activity. However estrogen (5mM) (p < 0.01) and testosterone (5mM) (p < 0.01) significantly upregulates the vasopressin stimulated hALC-1 promoter activity. Thus the full length promoter is required for hypertrophic activation of the hALC-1 gene.