Obstructive sleep apnea and aldosterone

Tagged with: Media

Posted on: June 1, 2009

Hypertension is elevated blood pressure in the arteries. Increased blood volume, increased heart rate and constriction of arterial blood vessels are some factors that can elevate pressure within the blood vessels. Hypertension can also occur in association with risk factors such as obesity, stress, a high fat or high sodium diet, a sedentary lifestyle, and in association with certain disorders such as Cushing's disease.

Hypertension usually has no symptoms until vascular changes have occurred in the heart, brain or kidneys. Vascular changes from untreated hypertension may result in stroke, heart attack or other cardiovascular problem, renal failure or death. For many people, drug treatment in combination with eliminating risk factors can reduce hypertension.

In a small percentage of people, hypertension is treatment-resistant, meaning the blood pressure remains high despite the use of several anti-hypertension drugs. Some research indicates that there is a high prevalence of obstructive sleep apnea (OSA) in people whose hypertension is resistant to treatment. Recent studies indicate that the steroidal hormone aldosterone may play a role in this association.

Aldosterone is secreted by the adrenal gland. One target organ for aldosterone is the kidney. As the level of aldosterone increases, the kidneys excrete decreased amounts of water in the urine resulting in body tissues retaining fluid. A consequence of fluid retention is that the volume of blood increases. This then can increase pressure within the arterial blood vessels and result in hypertension. Other researchers have noted an association between a high aldosterone level and OSA in hypertensive subjects. For example, David Calhoun and colleagues in their 2004 study noted that resistant hypertensive subjects who had a high risk of having undiagnosed OSA or who had previously been diagnosed as having OSA excreted more urinary aldosterone in a 24-hour period than did subjects who had a low risk of having undiagnosed OSA.

Dorthe Moller and colleagues noted that their OSA subjects had higher blood levels of aldosterone than did subjects without OSA. Further supporting a link between aldosterone levels and OSA is the finding that OSA treatment reduces aldosterone levels.

Scientists currently have no explanation why OSA is associated with an increased aldosterone level in people with resistant hypertension. One possibility that has been suggested is that OSA may stimulate angiotension II production which then stimulates the production of aldosterone.

Previously, researchers believed that hyperaldosteronism was a rare feature in people with hypertension since it apparently affected only 1 to 2 percent of people with hypertension. More recent studies are now suggesting that hyperaldosteronism may be more common and affect 6 to 20 percent of people with hypertension. An increase in the aldosterone level in people with resistant hypertension may result from undiagnosed OSA. Andrew Logan and colleagues found that 83 percent of people with resistant hypertension had undiagnosed OSA. Screening and treating resistant hypertensive patients for OSA may help lessen the likelihood of their suffering potentially life-threatening consequences of hypertension. More studies are needed to definitively prove a connection between aldosterone and OSA.

If there is a link, future studies may then determine whether OSA induces an increased aldosterone level or whether an increased aldosterone level induces OSA. If the former, studies would need to determine whether a person would benefit from treating OSA to reduce aldosterone levels; if the latter, whether a person would benefit from an aldosterone antagonist drug to reduce the severity of OSA. For now, scientists continue investigating the possible role of aldosterone in OSA.

by Regina Patrick RPSGT Regina Patrick is a Sleep Technologist at St. Vincent Mercy Sleep Center in Toledo, OH and appears regularly in Focus Journal.

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