Obstructive sleep apnea (OSA) is defined as episodes of blockage to the upper airways during sleep (minimum of 5 events per hour lasting at least 10 seconds). The episodes can be decreased breathing or even complete absence of breathing (apnea) during sleep. The most common form of apnea is when the throat muscles intermittent relax and block the airway during sleep. OSA has a strong association with risk of high blood pressure, cardiovascular diseases, and stroke. 

It’s estimated that about 75% of treatment-resistant hypertension may be from underlying sleep apnea.

The mechanisms for how people with sleep apnea can develop high blood pressure is complex, involving changes in fluid shifts, the renin-angiotensin-aldosterone system, and sympathetic/parasympathetic tone.

At night, fluid from the lower body gets redistributed to the neck, which causes further obstruction in the throat. The renin-angiotensin-aldosterone is a hormonal system that regulates BP, fluid, and electrolyte balance in the body. Low oxygen levels from apnea leads to increase activation of renin and thereby aldosterone, which increase fluid retention and can cause increased swelling of the muscles around the airways. The low oxygen levels activate the sympathetic nervous system (which produce adrenaline), which can cause increases in blood pressure.