Emerging evidence indicates that within the cardiovascular system, erythropoietin (Epo), has important non-erythropoietic functions in health and disease states. However, it is unknown if the heart is a producer of Epo, or if these effects occur due to circulating Epo. To study the functions of cardiac-derived Epo, a cardiomyocyte-specific Epo deletion mouse was created using cre/lox technology. Interestingly, this cardiomyocyte-specific deletion leads to an upregulation, not loss, of whole heart Epo expression. Using cellular sorting, we found that the remaining cardiomyocytes (~20% of the cardiomyocyte population where the Epo gene has not been deleted) were responsible for producing the Epo overexpression. Together, this thesis identifies the cardiomyocyte cells as an important source of Epo, and establishes that cardiac Epo expression is regulated in a distinct, tissue-specific manner.