Innate sleep apnoea in spontaneously hypertensive rats is associated with microvascular rarefaction and neuronal loss in the preBötzinger Complex

Abstract

AbstractSleep apnoea is a major threat to physical health and carries a significant economic burden. These impacts are worsened by its interaction with, and induction of, its comorbidities. Sleep apnoea holds a bidirectional relationship with hypertension which drives atherosclerosis, ultimately culminating in vascular dementia. To enable a better understanding of this sequalae of events, we investigated innate sleep apnoea in spontaneously hypertensive rats (SHRs), which have a range of cardiovascular disorders. SHRs displayed a higher degree of sleep disordered breathing, which emanates from poor vascular health leading to a loss of preBötC neurons. This model also displays small vessel white matter disease, a form of vascular dementia, likely associated with neuroinflammation in the hippocampus and the related deficits in both long- and short-term memory. Therefore, hypertension induces sleep apnoea through vascular damage in the respiratory column, culminating in neuronal loss in the inspiratory oscillator. This induction of sleep apnoea which in turn will independently exacerbate hypertension and neural inflammation, increasing the rate of vascular dementia.