Sleep disturbance among spontaneously hypertensive rats is mediated by an α1-adrenergic mechanism

Inadequate sleep may aggravate hypertension, but the pathophysiology of sleep disturbance in hypertension remains unknown. Among spontaneously hypertensive rats (SHR), sleep disturbance co-occurred with sympathetic hyperactivity; therefore, we hypothesized that the sleep disturbance can be alleviated by antagonizing the adrenergic overdrive.

Polysomnographic recording was performed in SHR by telemetry. The animals were first injected with saline, and 2 days later with a hypotensive agent. Cardiac and vascular sympathetic activity were assessed using the normalized low-frequency power (LF%) of heart rate variability and the low-frequency power of arterial pressure variability (BLF), respectively.

A comparison was made between the saline and hypotensive drug treatments. During quiet sleep (QS), the α1-blocker prazosin induced a significant decrease in BLF, but had no effect on LF%. The total time and bout duration of QS were lengthened and QS interruption was reduced (P < 0.05 for all). When both α1- and α2-adrenoceptors were blocked by phentolamine, both BLF and LF% were lower (P < 0.05 for both), but no modification to sleep structure could be observed. To antagonize β-adrenergic activity, atenolol and propranolol were injected. The LF% after either antagonist treatment was significantly decreased; however, sleep structure was not significantly changed. The QS-promoting effect of prazosin is specific to SHR, because prazosin is ineffective when administered to Wistar-Kyoto rats.

α1-adrenergic antagonism may reverse, at least partially, the poor sleep quality of SHR, suggesting a vicious cycle can be established between adrenergic overdrive and sleep disturbance.