Blocking Hypertension in Patients with Sleep Apnea
Obstructive sleep apnea (OSA) is a prevalent condition that affects one out of four Americans between the ages of 30 and 70 years. Unfortunately, it is frequently the cause of high blood pressure, or hypertension.
In the August 2016 issue of the journal, Science Signaling, new findings were published from researchers out of the University of Chicago that showed the cascade of signals that happens in this type of hypertension caused by OSA. They make suggestions about ways to disrupt the signals and prevent hypertensive episodes.
Leader of the study, Dr. Nanduri Prabhakar, and director of the Institute for Integrative Physiology and Center for Systems Biology of Oxygen Sensing at the University, notes that these results provide the mechanistic cause of OSA-related hypertension. The findings also offer a way to block hypertensive episodes and restoring normal blood pressures.
The link between hypertension and OSA starts in the carotid body, which is a cluster of cells inside the carotid arteries located on either side of the neck. The chemosensory cells in the carotid bodies measure blood oxygen levels and use it to regulate breathing. People with apnea have frequent starts and stops in breathing during sleep, so their oxygen levels decline significantly. The carotid bodies then release the messages to increase breathing rate to bring the oxygen back to normal in the bloodstream. Unfortunately, however, the signals also increase the blood pressure, which sometimes leads to having a stroke during sleep.
In both types of apnea (central and obstructive), the authors note, there are acute elevations in blood pressure that are linked to the apnea episodes. This further makes patients susceptible to hemorrhagic stroke, chronic hypertension, and heart failure. Therefore, it is vital to control hypertension in patients with sleep apnea, as it has become a major clinical concern.
Since this is such a concern, scientists mapped out the signaling cascades that start with sleep apnea and lead to the development of hypertension.
Apneic episodes lead to low oxygen levels in the blood, at which time the carotid bodies generate reactive oxygen species (the natural byproduct of oxygen metabolism). Heme oxygenase-2 is then deactivated, which is an enzyme that makes carbon monoxide, and this leads to higher hydrogen sulfide, a product that stimulates the carotid bodies and allows them to send signals throughout the body to make more oxygen.
Those signals also cause constriction of the blood vessels, which raises blood pressure. Standard hypertension therapies, Dr. Prabhakar notes, do not work for apnea-related hypertension.
Carotid bodies were first researched in the 1960s, in patients with asthma. Doctors found that removing the carotid bodies would treat the disease but cause sleep apnea. Even though removal of the carotid bodies prevented hypertension, the side effects were severe. Patients were unable to exercise much because they could not breathe more during exertion activities. Some of those patients died in their sleep after extended apneic episodes. Therefore, while the information was useful, it is not an option for treatment.
Instead, the scientists have suggested using medications to inhibit the cystathionine-y-lyase enzyme, which is needed to make hydrogen sulfide and signal the intake of oxygen. These drugs may be able to disrupt the network of signals that lead to sleep apnea-related hypertension.
Results suggest that the inhibition of that enzyme in order to reduce hydrogen sulfide signals in the carotid bodies may be the next approach to helping patients with apnea-related hypertension.
Rachael Herman is a professional writer with an extensive background in medical writing, research, and language development. Her hobbies include hiking in the Rockies, cooking, and reading.
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