High dietary sodium causes dyssynchrony of the renal molecular clock in rats.

Speed JS, Hyndman KA, Roth K, Heimlich JB, Kasztan M, Fox BM, Johnston JG, Becker BK, Jin C, Gamble KL, Young ME, Pollock JS, Pollock DM. High dietary sodium causes dyssynchrony of the renal molecular clock in rats. Am J Physiol Renal Physiol 314: F89-F98, 2018. First published September 27, 2017; doi:10.1152/ajprenal.00028.2017.-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 (ETB) receptor functions to facilitate Na+ 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 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 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 intrarenal circadian dyssynchrony mediated, in part, through activation of ETB receptors within the renal inner medulla.

Ability of near infrared spectroscopy to measure oxygenation in isolated upper extremity muscle compartments.

PURPOSE: Near infrared spectroscopy (NIRS), a noninvasive means for monitoring muscle oxygenation, may be useful in the diagnosis of acute compartment syndrome, a condition characterized by poor tissue perfusion. This study used the decrease in muscle oxygenation caused by exercise to investigate the ability of anatomic placement of NIRS sensor pads over compartments of the forearm to isolate perfusion values of a specific compartment. METHODS: We recruited 63 uninjured volunteers from a private clinic-based setting and placed NIRS sensor pads over the dorsal, volar, and mobile wad compartments of 1 forearm. A total of 49 participants also had the contralateral forearm monitored, which served as an internal control. Participants performed a series of 3 exercises designed to sequentially activate the muscles of each compartment. A washout period separated each exercise to allow perfusion to return to baseline. We compared NIRS values of each compartment recorded during muscle contraction with baseline values. RESULTS: Mean NIRS values decreased significantly from baseline during muscle contraction for all compartments, whereas mean NIRS values of muscle compartments that remained at rest showed little or no change. We observed no changes in NIRS values of the contralateral arm, which remained at rest during the entire data collection period. CONCLUSIONS: Although lack of an existing method for quantifying muscle perfusion precludes validation of this technique against a reference standard, this study suggests that NIRS can provide oxygenation values that are both sensitive and specific to muscle compartments of the forearm. Future studies should investigate NIRS among patients with upper extremity injuries. TYPE OF STUDY/LEVEL OF EVIDENCE: Diagnostic III.