Brain nitric oxide and inflammation in chronic intermittent hypoxia: Contributors to cognitive impairment and hypertension.

Chronic intermittent hypoxia (CIH) is a key feature of obstructive sleep apnea (OSA) and leads to physiological changes that can cause cardiovascular and neurological issues. This review explores the role of nitric oxide (NO) and inflammation in the development of CIH-induced health problems, specifically focusing on hypertension and cognitive dysfunction. We synthesize current evidence regarding how CIH modulates inflammatory processes and NO signaling in different brain regions, especially autonomic control centers crucial for cardiovascular regulation. We also discuss the activation of proinflammatory transcription factors, the generation of reactive oxygen species, and the involvement of pattern recognition receptors in CIH-induced neuroinflammation. Regarding cardiovascular changes associated with CIH, we focus on the effects of NO and inflammation in central autonomic regions such as the organum vasculosum of the lamina terminalis (OVLT), subfornical organ (SFO), median preoptic nucleus (MnPO), and paraventricular nucleus (PVN), shedding light on their contributions to sustained hypertension in CIH. The review delves into the latest findings on sex differences in CIH-induced neuroinflammation. In examining the current knowledge, we have pinpointed significant gaps in understanding, especially concerning the specific mechanisms of NO and inflammation interactions in different brain regions during CIH. This review provides insights into potential therapeutic targets and emphasizes the need for further research to develop more effective treatments for OSA-related cardiovascular and neurological complications.