Brainstem Warning Signals in Sleep Apnoea Drive Blood Pressure up

Photo by Andrea Piacquadio

In the US, nearly 40 million adults have sleep apnoea, and more than 30 million of them use a continuous positive airway pressure (CPAP) machine while sleeping. But the machines tend to be expensive, clunky and uncomfortable – resulting in many users giving up on using them.

Hypertension is often linked with sleep apnoea because the brain works harder to regulate blood flow and breathing during sleep. A recent study at the University of Missouri (Mizzou) offers new insight into the underlying mechanisms within the brain contributing to hypertension for those with sleep apnoea.

The findings, which are published in the Journal of Physiology, can help pave the way for new drugs that target the brainstem to bring blood pressure back down to normal levels for those with sleep apnoea.

The study took place in the lab of David Kline, a professor in Mizzou’s College of Veterinary Medicine and researcher at the Dalton Cardiovascular Research Center.

“When oxygen levels in the blood drop during sleep apnoea, the forebrain sends warning signals to the brainstem area that controls heart and lung functions,” Kline said. “By studying these signals, we found that two neurochemicals, oxytocin and corticotropin-releasing hormone (CRH), cause the brainstem to become overactive. Over time, this leads to hypertension.”

Hypertension leads to an increased risk of stroke, complications in the metabolism and a variety of other health issues.

“Not only do those with sleep apnoea often have high blood pressure, but they also lose a lot of sleep, they have more cognitive and memory issues, and they are more prone to injury at work due to sleepiness,” Kline said.

By being the first to identify the role that oxytocin and CRH play in strengthening and overexciting the pathways and mechanisms involved in sleep apnoea, Kline and his fellow researchers hope to pave the way for the design of better therapeutic approaches for humans and animals.

“Our ultimate goal is to eventually help clinicians develop specific drugs to target either these neurochemicals or the proteins they bind to in a way that reduces high blood pressure,” Kline said. “This discovery opens the door for future research to block the pathways these neurochemicals use, ultimately helping to bring blood pressure back to normal levels.”

Source: University of Missouri

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