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Obstructive Sleep Apnea (OSA) is generally considered a risk factor for hypertension. Up to 90% of OSA patients have hypertension, and 30-35% of hypertensive patients have OSA. Both rates, of course, are far above the prevalence of each disease in the general population. Acute apneas cause wide swings of blood pressure, especially high blood pressure just after the apnea ends; repetitive apneas not only induce these acute changes with each event but also a gradual rise in baseline blood pressure persisting even after the sequence of apneas ends. This occurs both in animals and humans, and supports the idea that OSA can cause sustained hypertension. There are several possible mechanisms for the acute rise in blood pressure with each apnea: lack of oxygen, stimulating chemoreceptors which increase activity of the heart and blood vessels; acute arousal from sleep itself; the extra muscular effort required to overcome the obstruction; and increased pressure within the thorax. However, the same type of blood pressure rise occurs with central apneas, suggesting that lack of oxygen may be the most important factor, or at least more important the increased muscular effort or thoracic pressure. The greater the oxygen desaturation, the more the blood pressure changes. Also, supplemental oxygen alleviates these blood pressuree rises. If the crucial trigger is hypoxia, then this probably acts to increase activity of the sympathetic nervous system, responsible for the emergency "fight-or-flight" stress reaction. This constricts blood vessels and increases cardiac output. Then the sharp rise in blood pressure at the end of the apnea may result from the sudden release of pressure in the thorax with the overcoming of obstruction, allowing an increase in cardiac output before the blood vessels have had time to relax. There is evidence that apnea itself, as well as hypoxia and excess carbon dioxide, can elicit increased sympathetic activity. But these acute changes are of less clinical concern than the chronic sustained increase of blood pressure. It has been shown that sympathetic overactivity will persist at least twenty minutes after respiration and cardiac activity return to normal following the end of breathing obstruction. In OSA patients who ended up having tracheostomies, before the surgery their urinary levels of the sympathetic brain hormone norepinephrine was elevated throughout the day, but after tracheostomy these returned to normal. A significant correlation has been observed between urinary norepinephrine and the respiratory disturbance index. It may take a long time for sustained daily hypertension to develop in human patients with OSA. Animal experiments generally use shorter-lived rats and allow 35 days for hypertension to develop. The rats are studied using chambers in which added nitrogen reduces oxygen levels, causing low arterial blood oxygen level of 70-80% in these rats. This induces acute blood pressure changes similar to those seen in humans after apneas. Using supplemental carbon dioxide can reproduce the experience of asphyxia, still more powerful in eliciting sympathetic activity. The fact that the human antiadrenergic antihypertensive drug prazosin can block most of this acute blood pressure response further implicates sympathetic overactivity. In chronic studies with this model, rats develop sustained increases in blood pessure which can be alleviated by various interventions to block sympathetic activity, such as carotid body denervation or peripheral sympathetic denervation. Differences in response among various strains of rat suggest the role of genetic factors. Recent experiments have continued to explore the idea that episodically low blood oxygen increases daytime blood pressure through chronic activation of the sympathetic nervous system. Blocking sympathetic innervation of the kidney will prevent this effect and also prevent rises in tissue norepinephrine. A similar prevention of hypertensive effect results from removal of the medulla of the adrenal gland, which secretes sympathetic hormones such as norepinephrine.

This article is less a primary research report such as we are used to reviewing than a review of a variety of research studies pertaining to the same issue, specifically the mechanism of acute and chronic blood pressure elevation due to apneas, low oxygen, and high carbon dioxide in a rat model of human sleep apnea. The evidence seems to point towards sympathetic nervous system activation by the apneas, the hypoxia, the high carbon dioxide, or all together. The resulting emergency "fight or flight" reaction of the body to dangerous situations includes such physiological changes as increased heart rate, increased cardiac output, and raised blood pressure. The author's explanation for why the most consistent and dramatic acute rise in blood pressure follows the end of the apnea is interesting--that the blood pressure already enhanced by increased vascular muscle activity is further enhanced by an increase in cardiac output due to a drop in intrathoracic pressure--but I am not convinced that this has as yet acquired the status of demonstrated fact. On the other hand, his argument that the episodic sympathetic overactivity associated with acute apneas eventually leads to persistent sympathetic overactivity causing higher blood pressure throughout the day seems very plausible, and supported by further animal research with antihypertensive medications that block sympathetic activity as well as surgical means of blocking sympathetic activation. The author draws little in the way of clinical implications from this research but one implication that I would draw is that anti-sympathetic antihypertensive drugs like prazosin should be quite as effective in hypertension secondary to OSA as in other varieties of hypertension. On the other hand, alternative antihypertensive drugs, such as diuretics, might be less effective. His model implies that the hypertension associated with OSA does not result mainly from the obesity also often associated with OSA, though of course the possibility exists that obesity may contribute its own component as well. Furthermore, the successful treatment of OSA without weight loss might well normalize blood pressure, although the chronicity of hypertension might operate to delay or even prevent this therapeutic process. My own experience was that, several years before I was diagnosed with OSA, I was diagnosed with and treated for hypertension. Efforts to lose weight through a cardiovascular fitness program--consisting of mainly of educational interventions about diet and exercise changes--proved ineffective. I turned out to require a few different antihypertensive medication trials before my blood pressure was controlled. Then my blood pressure normalized without medications shortly after I started CPAP, and before I lost about 40 pounds through the Nutrisystem program (which, in contrast to the cardiovascular fitness program, supplied most of the food one was to eat). Subsequently, after termination of Nutrisystem and giving up a strenuous exercise program, I regained that 40 pounds plus an additional 60 pounds--with the result that my blood pressure rose again despite continuing CPAP. Then it fell as I started to lose weight on an Optifast diet program (which again providing everything I consumed). I conclude from this experience that both OSA and obesity have played a role in my hypertension, and that antihypertensive medications, CPAP, and weight loss have all been helpful. I would like to note in passing that the association of hypertension with OSA may be the most significant factor in some of the most serious known complications of OSA--stroke and heart attacks. Furthermore, we should bear in mind that the state of chronic sympathetic overactivation postulated to exist in the hypertensive sleep apneic may have other consequences, not only to the physical but also to the emotional functioning of the individual.

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