Aim: 

The leptin hormone is produced by adipose tissue and modulates the hypothalamic pathways that control food intake and energy homeostasis. Mice lacking leptin are obese and show altered circadian rhythms of sleep and blood pressure. We investigated whether leptin deficiency impairs the sleep-dependent control of systolic blood pressure (SBP) in the circadian periods of light (rest) and darkness (activity).

Methods: 

Leptin-deficient B6.V-Lep^ob/OlaHsd obese mice (ob/ob, n = 6) and lean wild-type littermates (WT, n = 10) were implanted with microelectrodes for discriminating wake-sleep states and a telemetric blood pressure transducer (TA11PA-C10, DSI). Ten days later, recordings were performed for 3 days with the mice undisturbed and freely moving in their own cages. SBP was computed in episodes of wakefulness (W), non-rapid-eye-movement (non-REM) sleep, and REM sleep of duration >60 s in the light and dark periods. The mean value of SBP was analyzed with a 3-way analysis of variance and t-test with significance at p < 0.05.

Results: 

SBP significantly depended on interaction effects between and among 3 factors: wake-sleep state, light-dark period, and genetic group. On passing from W to non-REM sleep, SBP decreased significantly more in ob/ob than in WT mice. On passing from non-REM sleep to REM sleep, SBP significantly increased in WT but not in ob/ob mice. In non-REM sleep and REM sleep, SBP was significantly higher during the dark than during the light period in WT mice but not in ob/ob mice.

Conclusion: 

These data indicate that both sleep-related and circadian factors underlie the altered regulation of SBP, which is associated with congenital leptin deficiency in ob/ob mice. The results thus suggest that the hypothalamic control of energy homeostasis is linked with the circadian and the sleep-dependent control of blood pressure.