Dyssynchrony of circadian rhythms are associated with various disorders, including cardiovascular and metabolic diseases. The cell autonomous molecular clock maintains circadian control, however, environmental factors that may cause circadian dyssynchrony either within or between organ systems are poorly understood. Our lab recently reported that the endothelin B (ETB) receptor functions to facilitate Na+ excretion in a time of day dependent manner. Therefore, the current study was designed to determine whether high salt (HS) intake leads to circadian dyssynchrony within the kidney, and whether the renal endothelin system contributes to control of the renal molecular clock. We observed that HS feeding led to region-specific alterations in circadian clock components within the kidney. For instance, HS caused a significant 5.5-hour phase delay in the peak expression of Bmal1 and suppressed Cry1 and Per2 expression in the renal inner medulla, but not the renal cortex, of control rats. The phase delay in Bmal1 expression appears to be mediated by endothelin (ET-1) because this phenomenon was not observed in the ETB deficient rat. In cultured inner medullary collecting duct cells, ET-1 suppressed Bmal1 mRNA expression. Furthermore, Bmal1 knockdown in these cells reduced epithelial Na+ channel expression. These data reveal that HS feeding leads to intra-renal circadian dyssynchrony mediated, in part, through activation of ETB receptors within the renal inner medulla.