Obstructive Sleep Apnoea and Hypertension: the Role of the Central Nervous System

Abstract

Recent human brain imaging investigations and, in particular, combined microneurography recording of resting sympathetic activity with high-resolution functional magnetic resonance imaging have provided some important insights into changes in brain function and anatomy associated with resting sympathetic activity. Functional and anatomical changes occur in OSA, including in regions of the brainstem circuitry known to be responsible for setting resting sympathetic activity. Furthermore, these changes are reversed following continuous positive airway treatment in concert with reductions in resting sympathetic drive. These resent findings suggest that the central changes may contribute significantly to the hypertension associated with OSA.

Clinical and prognostic significance of a reverse dipping pattern on ambulatory monitoring: An updated review

“…Notably, day‐night BP difference in the whole study population was inversely related to sympathetic nerve traffic ( r =−.76, P <.0001), suggesting that sympathetic activation in human hypertension may potently affect circadian BP variations . Also, in patients with obstructive sleep apnea, a condition frequently associated with nocturnal hypertension, increased sympathetic tone responsible for BP elevations during apneic episodes has been documented in microneurographic studies …”

“…12 Also, in patients with obstructive sleep apnea, a condition frequently associated with nocturnal hypertension, increased sympathetic tone responsible for BP elevations during apneic episodes has been documented in microneurographic studies. 13 Impaired renal capacity to excrete sodium has been shown to be a factor leading to a blunted nocturnal BP fall. 14 This condition has been associated with reduced daytime sodium excretion, and the nocturnal BP increase via the pressure-natriuresis mechanism is a likely compensatory mechanism to increase sodium excretion and preserve sodium balance.…”

Erythropoietin, a putative neurotransmitter during hypoxia, is produced in RVLM neurons and activates them in neonatal Wistar rats

“…These results explain some of the mechanisms of hypertension induced by hypoxia. Hypertension due to increased sympathetic nerve activity has been shown in patients with hypoxia ( 8 ), and we think that EPO in the RVLM neurons plays an important role in these patients.…”

“…Patients with hypoxia often exhibit high blood pressure (BP) and increased sympathetic nerve activity ( 8 ). Furthermore, chronic hypoxia reportedly induces a high BP ( 12 ), and a significant correlation in the oxygen partial pressure (P o 2 ) is present between blood and cerebrospinal fluid ( 30 ).…”

Joint interaction effect of metabolic syndrome and obstructive sleep apnea on hypertension

“…Hypertension has a strong relationship with OSA . Hypertension induced by OSA occurs via chronic intermittent hypoxia in accordance with certain pathological mechanisms, such as overactivation of the sympathetic nervous system, endothelial dysfunction, and renin–angiotensin–aldosterone system dysfunction, ultimately increasing the risk of cardiovascular morbidity and mortality . However, it remains unclear whether metabolic syndrome (MS) plays a role in the well‐established mechanisms that accelerate the detrimental effects of OSA on hypertension .…”