Dyssynchrony of circadian rhythms is 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 laboratory recently reported that the endothelin (ET-1) B ([ET.sub.B]) receptor functions to facilitate [Na.sup.+] excretion in a time of day-dependent manner. Therefore, the present 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-h phase delay in the peak expression of Bmall and suppressed Cry1 and Per2 expression in the renal inner medulla, but not the renal cortex, of control rats. The phase delay in Bmall expression appears to be mediated by ET-1 because this phenomenon was not observed in the [ET.sub.B]-deficient rat. In cultured inner medullary collecting duct cells, ET-1 suppressed Bmall mRNA expression. Furthermore, Bmall knockdown in these cells reduced epithelial [Na.sup.+] channel expression. These data reveal that HS feeding leads to intrarenal circadian dyssynchrony mediated, in part, through activation of [ET.sub.B] receptors within the renal inner medulla. circadian rhythm; dyssynchrony; Bmall; kidney; salt doi: 10.1152/ajprenal.00028.2017.