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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep-related respiratory disorders are mainly represented by the consequences of partial or total upper airway obstruction during sleep, which lead to clinical pictures ranging from "pure" snoring to full-blown obstructive sleep apnea syndrome, including obstructive sleep hypopnea syndrome and upper airway resistance syndrome. These pictures share symptoms like snoring and excessive daytime sleepiness. Beyond the social and professional impairment and the increased risk of traffic and work accidents, these patients are exposed to the complications of systemic hypertension, which is often associated, and of less frequent cardiorespiratory failure. The diagnosis is based upon polysomnography which demonstrates the ventilation abnormalities. Since stable weight loss is most often impossible to obtain, the treatment of choice is based on nasal continuous positive airway pressure during sleep. In some selected cases, facial bone surgery may be helpful.
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PMID:[Sleep-related respiratory disorders]. 903 29

Obstructive sleep apnea is a common breathing problem that results in recurrent episodes of nighttime hypoxemia, hypercapnia, bradytachycardia, and hypertension, as well as sleep disturbance and daytime hypersomnolence. The obstruction is located in the oropharynx and is caused by hypotonia of the pharyngeal dilator muscles. In this paper, the various mechanisms affecting motor output to the upper airway muscles are reviewed. In particular, the respiratory function of the pharyngeal dilator muscles, the various reflex mechanisms underlying their control, and the effects of sleep on these mechanisms are discussed. The literature relevant to the central neuronal circuits and neurotransmitters that may be involved in the state-dependent activity of the pharyngeal dilator muscles is also reviewed. In addition to an examination of these basic mechanisms, consideration is given throughout this review as to how these mechanisms may relate to the normal control of pharyngeal patency awake and asleep and how they may be involved in the pathogenesis of obstructive sleep apnea.
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PMID:Motor control of the pharyngeal musculature and implications for the pathogenesis of obstructive sleep apnea. 908 93

Episodes of sleep disordered breathing are surprisingly common in asymptomatic, middle-aged individuals. The majority of these events are hypopneas, rather than apneas. Even though these events cause rather modest decreases in arterial oxygen saturation, they evoke substantial increases in arterial pressure. In this population, mild to moderate sleep disordered breathing is associated with elevated daytime blood pressure. The mechanisms responsible for the acute and chronic cardiovascular effects of sleep disordered breathing are incompletely understood. Chemoreflex mechanisms appear to be more important than intrathoracic pressure changes in causing the acute elevation in arterial pressure that occurs after obstructive sleep apnea. Arousal from sleep may contribute to this pressor response, either in an additive or synergistic manner. Relatively brief exposure to combined hypoxia and hypercapnia during wakefulness can produce an increase in sympathetic outflow to skeletal muscle that persists after return to room air breathing. This lingering post-asphyxic effect on sympathetic outflow may be the basis of chronically elevated sympathetic nervous system activity which accompanies sleep apnea syndrome and may contribute to sustained hypertension in these individuals.
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PMID:Acute and chronic cardiovascular responses to sleep disordered breathing. 908 12

The systemic arterial blood pressure response to obstructive sleep apnea (OSA) in humans is usually repetitive (with each apnea) acute elevation with return to near baseline following the apnea. In addition, it is believed by most investigators that chronic diurnal elevation of systemic blood pressure may result from repetitive nightly apneas in humans, resulting in systemic hypertension in about 50-70% of sleep apnea patients. Mechanisms of the chronic elevation in blood pressure are difficult to investigate in humans because it may take many years of repetitive apneas for sustained daytime blood pressure to develop. The rat is an especially good animal to use to investigate these mechanisms because of its use as a model in many types of hypertension. The authors have examined the response to chronic episodic hypoxia (for 35 consecutive days) in several strains of rats, discovering that systemic blood pressure (BP) remains chronically elevated in the absence of hypoxic stimulation after this period. This manuscript reviews the findings in this model after various interventions in the neurochemical and neuroendocrine mechanisms controlling BP in this animal.
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PMID:The rat as a model of chronic recurrent episodic hypoxia and effect upon systemic blood pressure. 908 13

There exist real and potential links between the risk factors for and co-morbidity associated with diabetes and sleep apnea. The common occurrence of obesity, hypertension, and disorders of metabolism in each disease is but one example. While the occurrence of sleep apnea with glucose intolerance or insulin resistance could present sampling bias or intersection of common human diseases, an alternative hypothesis is that the events in obstructive sleep apnea (OSA) trigger different, perhaps unique, adaptations in metabolic processes involving insulin action and glucose regulation. Further, clinical studies can be designed to define the extent and potential mechanisms for alterations in insulin and glucose levels in OSA and to determine the sample size and power for a longitudinal study that would follow the relative rates of progression of obesity (including neck size as a body characteristic), breathing abnormalities during sleep, insulin sensitivity, and subsequent risk for non-insulin-dependent diabetes mellitus (NIDDM) and/or symptomatic OSA.
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PMID:Diabetes and sleep apnea. 908 17

For about 120 years we have been looking for the 'cause' of essential hypertension. It is possible that we have merely been wandering through its graveyard, looking at the pathogenetic mechanisms but never the actual cause? Here we pass the gravestone of increased sympathetic activity; there the gravestone of low renin activity. Here high endothelin; there low EDRF. Here high thromboxane A2; there low prostacyclin. It is possible that all these and so many other pathogenetic factors are all due to one basic defect? Is it possible that, in the dead of night while patients with EH have been sleeping, the villain has been lurking in their mouths, stuck somewhere at the back of their throats, hidden from view yet choking them hundreds of times a night. But this intermittent strangulation has not occurred silently. On the contrary, it has made its presence felt in the most irritating way, with snores, groans, grunts, gasps and frightening periods of total apnea. But we, their physicians, never asked about these symptoms, or, if we did, we never paid heed to them. This is clear from the fact that, most cases of OSA occur in association with EH yet are not diagnosed. Perhaps the next 'arousal response' should be the arousal of physicians' consciousness so that they can at long last wake up to the existence of the close connection between sleep-related breathing disorders and hypertension and breathe some new life into the treatment of two old diseases-essential hypertension and secondary hypertension. Early diagnosis and treatment of the sleep-related breathing disorders may not only make the patient feel much better, (something our antihypertensive medications do not always do), but may reduce the blood pressure and prevent the progression of renal and cardiovascular damage as well.
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PMID:Sleep-related breathing disturbances: their pathogenesis and potential interest to the nephrologist. 914 Sep 93

The increasing prevalence and far-reaching medical, social, and economical implications of obesity have made it a national health-care crisis in the United States. About one in every three persons is at least 20% above "ideal" body weight, and approximately 5% have direct weight-related serious health problems (morbid obesity), including hypertension, hyperlipidemia, coronary artery disease, adult-onset diabetes mellitus, degenerative osteoarthropathy, and obstructive sleep apnea. Morbidly obese patients have an estimated 6- to 12-fold increase in mortality. In addition, they have a substantially diminished quality of life, not only physically but also psychosocially due to overt and occult prejudice. Weight reduction must be aggressively pursued in these patients. Medically supervised weight-control programs have been ineffective because patients cannot maintain pronounced long-term weight loss. In contrast, current operative methods have been proved to be effective in helping patients achieve and maintain permanent weight reduction. Several operations have been designed and assessed; with these procedures, weight loss is achieved by inducing malabsorption, maldigestion, early satiety, or a combination of these outcomes. Although these operations have associated side effects and limitations, the expected benefits outweigh the risks. For optimal results, patients must be carefully selected and treated by a multidisciplinary group.
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PMID:Surgical treatment of obesity: who is an appropriate candidate? 917 40

Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n = 10) and hypercapnia (n = 6), respectively. Plasma alcohol increased from 0 to 23.2 +/- 1.5 mmol/L (107 +/- 7 mg/dL) at 60 minutes and 20.2 +/- 1 mmol/L (93 +/- 4 mg/dL) at 85 minutes after alcohol intake (P < .0001). Alcohol induced an increase in heart rate from 59 +/- 2 to 66 +/- 2 beats per minute (P < .01) and increased the ratio of low- to high-frequency variability of heart rate (P < .05). Although alcohol increased sympathetic nerve activity by up to 239 +/- 22% of baseline values (P < .01), forearm vascular resistance after alcohol was lower than that after vehicle (P < .05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4 +/- 1% lower than it was during hypoxia after vehicle (P < .05) although arterial blood PO2 was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.
Hypertension 1997 Jun
PMID:Effects of alcohol on sympathetic activity, hemodynamics, and chemoreflex sensitivity. 918 Jun 29

We investigated the efficacy of an Angiotensin Converting Enzyme [ACE] inhibitor on daytime and night-time blood pressure in 55 male hypertensive patients with moderately severe to severe obstructive sleep apnea. We resolved to determine if treatment oriented towards the reduction of hypertension would be successful, despite persistent repetitive hypoxemia and sleep-disordered breathing. The study was a randomized, double-blind, single daily dose, placebo-controlled protocol, with 8 days drug intake (placebo or 2.5 mg Cilazapril) and monitoring on the final day of drug administration. Subjects underwent continuous 24-h arterial blood pressure monitoring during baseline and treatment conditions. Polysomnography was performed at night during the 24-h arterial monitoring period. Cilazapril (2.5 mg) lowered systolic, diastolic and mean blood pressure, despite persistence of repetitive obstructive apneas during sleep and the associated repetitive hypoxemia. The lowering of blood pressure occurred without a significant change in heart rate, and was noted during nocturnal sleep, performance testing and graded exercise.
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PMID:Effect of angiotensin converting enzyme inhibition [Cilazapril] on blood pressure recording in hypertensive obstructive sleep apneic patients. 929 11

Patients with untreated sleep apnea syndrome have a higher cardiovascular mortality. It is not known which mechanisms lead to this increase in mortality and whether it is independent from the often associated coronary heart disease and systemic hypertension. In 48 consecutive patients with coronary heart disease confirmed by angiography, exercise-ECG, Holter-ECG, echocardiography, spirometric tests, analysis of ventricular late potentials, heart rate variability and a test for sleep-disordered breathing with a screening device were performed. Seventeen patients showed disordered breathing during sleep (obstructive sleep apnea) with a desaturation index of > or = 10 (mean desaturation index 17.3 +/- 9.3 vs. 2.6 +/- 3.1 in the patients without sleep-disordered breathing). There are no significant differences in age (58.9 +/- 6.1 vs. 59.7 +/- 7.6 years), body-mass-index (28.6 +/- 3.7 vs. 27.7 +/- 3.3 kg/m2), left ventricular ejection fraction (57.2 +/- 13.6 vs. 64.0 +/- 14.6%), forced expiratory volume in 1 second/vital capacity 95.4 +/- 13.9 vs. 92.9 +/- 11.2% predicted, heart rate variability (standard deviation of the RR-intervals 39.4 +/- 29.4 vs. 37.2 +/- 17.0 ms), the frequency of premature ventricular beats over 24 h and at night, the frequency of multivessel disease (71 vs. 68%), additional hypertension 53 vs. 48%), status postmyocardial infarction (47 vs. 48%) and positive late potential analysis (24 vs. 13%). There were no ST segment depressions during the night. Patients with coronary heart disease and mild sleep-disordered breathing show no significant differences in the investigated parameters compared with patients without obstructive sleep apnea or sleep-disordered breathing.
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PMID:[Prognostically relevant parameters in patients with coronary heart disease, arterial hypertension and sleep apnea disorders]. 933 91


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