Study Unveils Brain Mechanisms Linking Sleep Apnea to Hypertension

A recent study out of the University of Missouri sheds new light on the complex relationship between sleep apnea and high blood pressure. Led by David Kline from the College of Veterinary Medicine, the team identified key neurochemicals in the brain that contribute to hypertension in individuals with sleep apnea. 

The study, published in The Journal of Physiology, reveals that when oxygen levels drop during sleep apnea episodes, the forebrain sends warning signals to the brainstem. Two specific neurochemicals play a crucial role in this process. "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," Kline explained. 

This discovery is particularly significant given the prevalence of sleep apnea in the United States, affecting nearly 40 million adults. The condition not only leads to high blood pressure but also impacts cognitive function, memory, and workplace safety due to sleepiness.

The researcher's findings open up new possibilities for targeted drug development. "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. 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,” Kline stated.