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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One of the major manifestations of obstructive sleep apnea is profound and repeated hypoxia during sleep. Acute hypoxia leads to stimulation of the peripheral chemoreceptors, which in turn increases sympathetic outflow, acutely increasing blood pressure. The chronic effect of these repeated episodic or intermittent periods of hypoxia in humans is difficult to study because chronic cardiovascular changes may take many years to manifest. Rodents have been a tremendous source of information in short- and long-term studies of hypertension and other cardiovascular diseases. Recurrent short cycles of normoxia-hypoxia, when administered to rats for 35 days, allows examination of the chronic cardiovascular response to intermittent hypoxia patterned after the episodic desaturation seen in humans with sleep apnea. The result of this type of intermittent hypoxia in rats is a 10- to 14-mmHg increase in resting (unstimulated) mean blood pressure that lasts for several weeks after cessation of the daily cyclic hypoxia. Carotid body denervation, sympathetic nerve ablation, renal sympathectomy, adrenal medullectomy, and angiotensin II receptor blockade block the blood pressure increase. It appears that adrenergic and renin-angiotensin system overactivity contributes to the early chronic elevated blood pressure in rat intermittent hypoxia and perhaps to human hypertension associated with obstructive sleep apnea.
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PMID:Invited review: Physiological consequences of intermittent hypoxia: systemic blood pressure. 1124 66

By using an inspired oxygen fraction that produces oxyhemoglobin desaturation equivalent to that seen in human sleep apnea, we have demonstrated that 35 days of recurrent episodic hypoxia (every 30 s for 7 h/day) results in an 8-13 mmHg persistent increase in diurnal systemic mean arterial blood pressure (MAP) in rats. Blockade of angiotensin II receptors (AT(1a)) eliminates this response. Separate groups of male Sprague-Dawley rats were fed high-salt (8%), ad libitum-salt, or low-salt (0.1%) diets for 7 wk: 2 wk of wash-in for baseline blood pressure measurement and 5 wk of experimental conditions. Rats in each salt group were subjected to episodic hypoxia whereas controls remained unhandled under normoxic conditions. MAP remained at basal levels in all nonepisodic hypoxia controls as well as high-salt-diet episodic hypoxia-exposed rats. Ad lib and low-salt episodic hypoxia rats showed an increase in MAP from 106 and 104 mmHg at baseline to 112 and 113 mmHg, respectively (P < 0.05). Whole kidney renin mRNA was suppressed in high-salt controls and episodic hypoxia rats, whereas kidney AT(1a) mRNA showed opposite changes. Suppression of the renin-angiotensin system with a high-salt diet blocks the increase in MAP in episodic hypoxia-challenged rats, in part by suppressing local tissue renin levels. Upregulation of the tissue angiotensin II system appears to be necessary for the chronic blood pressure changes that occur from episodic hypoxia.
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PMID:Blood pressure response to chronic episodic hypoxia: the renin-angiotensin system. 1179 74

The obesity epidemic is driving metabolic (insulin resistance) syndrome-related health problems including an approximately threefold increased coronary heart disease risk. Sympathetic hyperfunction may participate in the pathogenesis and complications of the metabolic syndrome including higher blood pressure, a more active renin-angiotensin system, insulin resistance, faster heart rates, and excess cardiovascular disease including sudden death. Possible factors augmenting sympathetic activation in the metabolic syndrome include alterations of insulin, leptin, nonesterified fatty acids (NEFAs), cytokines, tri-iodothyronine, eicosanoids, sleep apnea, nitric oxide, endorphins, and neuropeptide Y. Of note, high plasma NEFAs are a risk factor for hypertension and sudden death. In short-term human studies, NEFAs can raise blood pressure, heart rate, and a(1)-adrenoceptor vasoreactivity, while reducing baroreflex sensitivity, endothelium-dependent vasodilatation, and vascular compliance. Efforts to further identify the mechanisms and consequences of sympathetic dysfunction in the metabolic syndrome may provide insights for therapeutic advances to ameliorate the excess cardiovascular risk and adverse outcomes.
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PMID:Insulin resistance and the sympathetic nervous system. 1272 58

Hypertension resistant to 2 antihypertensive drugs is more common among obese patients than among lean patients. The case we describe and the observations we report suggest that refractoriness among obese hypertensives is frequently caused by obstructive sleep apnea and/or inappropriately high plasma aldosterone levels. In other words, obese hypertensives may have sleep apnea, obese hypertensives without sleep apnea may have inappropriately elevated levels of plasma aldosterone, and a surprising number of obese patients with sleep apnea also have elevated levels of aldosterone. The mechanisms by which obesity and obstructive sleep apnea increase aldosterone levels and raise blood pressure are not understood, but sympathetic nervous system activation and production of nonclassical adrenal stimuli are two possibilities. Obstructive sleep apnea can be detected with a careful history and various sleep studies. Inappropriately elevated aldosterone levels can be detected by measuring the ratio of plasma aldosterone concentration to plasma renin activity. Successful treatment of these resistant hypertensives often can be achieved by devices that provide positive pressure to the upper airway to correct obstructive sleep apnea and by incorporating an aldosterone antagonist in the therapeutic regimen.
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PMID:Resistant hypertension, obesity, sleep apnea, and aldosterone: theory and therapy. 1473 21

Sleep apnea syndrome (SAS) in patients with chronic heart failure (CHF) increases the risk of death. SAS was divided into 4 types: obstructive sleep apnea-hypopnea syndrome (OSAHS), upper airways resistance syndrome (UARS), central sleep apnea syndrome (CSAS), and sleep hypoventilation syndrome (SHVS). CSAS is caused by temporary cessation of central drive to respiratory muscles, OSAHS results from partial or complete collapse of the pharynx, UARS have typical symptoms of OSAHS and no changes on polysomnography, whereas SHVS results from pathological PCO2 increase with subsequent hypoxemia. Increase in sympathetic activity, renin-angiotensin-aldosterone activation, impaired baroreflex and tonic vagal heart rate control are markers of increased risk of sudden death. CSAS is frequent in patients with CHF. Decreased cardiac output causes delayed transmission of changes in arterial blood gas tensions from the lungs to the chemoreceptors. Increase chemoreceptor sensitivity results from hypoxia and pulmonary congestion. Both types of apneas (OSAHS and CSAS) may occur in the same patient. Periodic cessation in central drive to respiratory muscles (CSAS) causes obstructive apneas/hypopneas by decreased tone of pharyngeal muscles and their collapse. Obstructive apneas (OSAHS) may lead to central apneas by frequent arousals, decreased left ventricular function and prolongation of circulation. Treatment of SAS is based on improvement of cardiovascular function, nocturnal supplementation of O2 and various forms of noninvasive positive airway pressure (i.e. CPAP).
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PMID:[Sleep apnea syndrome in patients with chronic heart failure]. 1530 26

Obstructive sleep apnea (OSA) is the most common form of sleep-disordered breathing and frequently coexists with obesity. Almost 15 million Americans are affected by this disorder. This prevalence is likely increasing, given the current epidemic of obesity. Recent data confirm an association between sleep apnea and several cardiovascular disease conditions, suggesting that OSA may be a new risk factor for coronary artery disease, heart failure, heart rhythm disturbances and hypertension, independent of body mass index. In this review, the authors focus on the nature of the association between OSA and hypertension, the evidence suggesting a causal interaction, and discuss the potential pathophysiologic mechanisms responsible. These mechanisms include activation of the sympathetic and renin-angiotensin-aldosterone systems (RAAS), oxidative stress, and systemic and vascular inflammation, all of which could link OSA to a sustained increase in blood pressure. The authors also review potential therapeutic strategies for the hypertensive patient with OSA.
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PMID:Sleep apnea and hypertension. 1582 43

The obstructive sleep apnoea syndrome (OSAS) is caused by upper airway collapse during sleep. These episodes are associated with recurrent oxyhaemoglobin desaturations and arousals which lead to disruption of the sleep pattern and cognitive deterioration. Factors such as age, male sex, menopause, tobacco and alcohol consumption and anatomic abnormalities are demonstrated risk factors for OSAS development. Obesity, specially of abdominal type, is also a very strong predictor of OSAS, increasing the risk of apnoea by ten times. OSAS prevalence may reach 80% and 50% en males and females with morbid obesity respectively. OSAS induces sympathoexcitation, insulin resistance, renin-angiotensin system activation, oxidative stress, endothelial dysfunction, hypercoagulability and reduction of fibrinolysis leading to hypertension and increased cardiovascular risk. The best diagnostic procedure is polysomnography. Obesity treatment is followed by a dramatic improvement in OSAS. Weight loss of 10% results in reductions of apnoea index by 26%. Application of a positive pressure system is a very effective treatment for OSAS which reduces the apnoea index and improves cardiovascular risk and cognitive impairment.
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PMID:[The obstructive sleep apnoea syndrome in obesity: a conspirator in the shadow]. 1538 14

Hypertension is a very common comorbidity in patients with Cushing's disease/syndrome, resulting from the interplay of several pathophysiologic mechanisms, including stimulation of mineralocorticoid and glucocorticoid receptors as well as the associated insulin resistance, sleep apnea, and overexpression of renin-angiotensin system. Although treatment of Cushing's disease results in resolution or amelioration of hypertension in these patients, a significant proportion of patients do not achieve complete cure or require a prolonged period of time for complete response to therapy. Therefore, therapeutic strategies for Cushing's-specific hypertension are necessary to decrease morbidity and mortality associated with this disease. In this review, we discuss the pathophysiology of hypertension in patients with Cushing's disease, highlighting the therapeutic options, including the exciting new developments in the role of peroxisome proliferator-activated receptor (PPAR)-g agonists in the management of this patient population.
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PMID:Hypertension in patients with Cushing's disease: pathophysiology, diagnosis, and management. 1591 97

The Eighth European Meeting on Hypertension, held in Milan, Italy, was attended by approximately 4000 people. The programme consisted of 120 presentations, 337 poster sessions, 6 invited lectures/debates (endothelin antagonists; cardiac renin-angiotensin system; cancer and hypertension; adducin; angiotensin converting enzyme (ACE) gene polymorphism; pulse pressure) and 2 plenary sessions on 'sleep apnea and hypertension' and 'treatment of hypertension in the elderly'.
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PMID:Eighth European meeting on hypertension. 1598 69

The activation of adrenergic and renin-angiotensin-aldosterone (RAA) systems observed in patients with obstructive sleep apnoea syndrome (OSA) strongly affects functional status of the cardiovascular system. In this paper we discuss the link between obstructive sleep apnoea syndrome and common cardiovascular diseases such as systemic and pulmonary hypertension, ischaemic heart disease, stroke, arrhythmia and ventricular hypertrophy. We also present the importance of early pharmacologic treatment in preventing cardiac hypertrophy and ventricular dysfunction in patients with obstructive sleep apnoea syndrome.
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PMID:[Cardiovascular abnormalities in patients with obstructive sleep apnoea syndrome]. 1599 58


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