With obstructive sleep apnea, the upper throat closes and patients stop breathing numerous times during the night, putting them at risk for developing vascular disease that causes a treatment-resistant form of high blood pressure.
Nancy Kanagy, PhD, a professor in the UNM Department of Cell Biology and Physiology, is seeking to understand how that happens.
Just how sleep apnea worsens blood pressure is not well understood, but up to one in five people may suffer from it. When the National Institutes of Health put out a call for proposals on sleep apnea research several years ago, Kanagy realized UNM’s experience in conducting vascular studies could provide a novel approach.
“Most researchers were looking at the sympathetic nervous system,” Kanagy says. “We thought, ‘Why not develop a model to investigate vascular changes and contributions to the elevated blood pressure?’”
Kanagy’s team first developed a rat model of sleep apnea and found that it only takes about 14 days for repeated exposure to hypoxia (low oxygen) during sleep to increase blood pressure, even during waking hours. They found that hypoxia increases production of an artery-constricting peptide called endothelin, which elevates blood pressure. Ongoing studies are investigating exactly how that happens.
The team is also investigating hydrogen sulfide’s (H2S) role in controlling blood pressure. Sleep apnea patients show significantly lower H2S levels compared with normal sleepers. The molecule seems to limit inflammation and open arteries, leading to many positive effects in the cardiac and vascular systems.
“Long-term, we are hoping that a better understanding of these mechanisms will lead to new and more effective therapies to treat cardiovascular disease in sleep apnea patients,” Kanagy says.