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

Excessive nocturnal diuresis and natriuresis have been reported in patients with sleep apnea. The mechanisms responsible for these alternations in nocturnal renal function have not been clearly identified. To gain further insight into this matter, we studied 12 patients (one woman) with a mean +/- SD age of 50 +/- 9 yr and body mass index of 36.9 +/- 8.6 kg/m2. Polysomnography showed in all a sleep apnea syndrome with an apnea-hyponea index (AHI) of 81.3 +/- 41.7. Treatment with nasal continuous positive airway pressure (nCPAP) resulted in an AHI of 19.4 +/- 13.7 and in normalization of sleep characteristics. Diurnal renal function was normal in all subjects. Although untreated, patients showed an abolition of the well-known decrease in diuresis and natriuresis during the night (diurnal and nocturnal diuresis 56.3 +/- 26.8 and 77.2 +/- 33.4 ml/h, respectively, p = NS; diurnal and nocturnal fractional urinary Na+ excretion 0.42 +/- 0.09 and 0.70 +/- 0.55 ml/100 ml glomerular filtration [GF], respectively, p = NS). Results of nocturnal studies under nCPAP therapy showed a significant decrease in diuresis and natriuresis (nocturnal diuresis before and under nCPAP, respectively: 90.4 +/- 27.3 and 70.6 +/- 25.1 ml/h, p less than 0.02; nocturnal fractional urinary sodium excretion before and under nCPAP, respectively: 0.76 +/- 0.53 and 0.44 +/- 0.37 ml/100 ml GF, p less than 0.03). Morning blood levels of renin, aldosterone, antidiuretic hormone, epinephrine, and atrial natriuretic factor showed no significant difference before and under nCPAP, whereas norepinephrine significantly decreased from 309.5 +/- 104.2 before to 230.4 +/- 88.4 pg/ml under nCPAP (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diurnal and nocturnal diuresis and natriuresis in obstructive sleep apnea. Effects of nasal continuous positive airway pressure therapy. 843 Sep 77

Recent studies about renal function and volume regulating hormones in obstructive sleep apnea (oSAS) indicate complex disturbances in volume homeostasis. Increased nocturnal secretion of atrial natriuretic peptide (ANP) and decreased renin secretion during apnea looks similar to a situation seen during hypervolemia or increased cardiac volume load. Increased venous return induced by pathologically high negative intrathoracic pressure during obstructive apnea may be the cause. Since during wakefulness no true hypervolemia is present, a "pseudohypervolemia" or "central hypervolemia" must exist caused by volume shift from the peripheral to the central compartment during apnea. Since volume homeostasis and blood pressure regulation are complexly connected the question arises whether disturbances in volume homeostasis play a role in the pathogenesis of arterial hypertension in sleep apnea. In a subgroup of hypertensive patients hypertension is salt-sensitive and volume dependent; it is called volume-expanded or low-renin hypertension. An inhibitor of the Na+/K(+)-ATPase acting via the digitalis receptor - called digitalis like factor (DLF) - is regarded as the causative agent for the development of hypertension in these cases. From this background, we were interested in the question whether DLF may be the linkage between disturbances in volume homeostasis and the pathogenesis of hypertension in sleep apnea. We could demonstrate a decrease of nocturnal urinary excretion of DLF during nasal continuous positive air pressure (nCPAP) therapy. Since a positive correlation between changes in diuresis respectively natriuresis and DLF excretion was found, we suggested DLF to be involved in changes of renal function in sleep apnea besides ANP. In 3 patients we measured nocturnal plasma levels of DLF and renin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbances in volume regulating hormone system--a key to the pathogenesis of hypertension in obstructive sleep apnea syndrome? 165 Sep 45

1. It has recently been shown that obstructive sleep apnoea (OSA) patients have increased urinary water and salt excretion during sleep which tends to normalize with nasal continuous positive airway pressure (CPAP) treatment. 2. To investigate the mechanisms of these changes in renal function, nocturnal urinary excretion of catecholamines and guanosine 3':5'-cyclic monophosphate (cyclic GMP), which reflects atrial natriuretic factor (ANF) release, and next-morning plasma active renin concentrations were studied in 21 OSA patients on 2 consecutive nights, either untreated or treated with nasal CPAP. 3. In keeping with previous results, fractional urine flow and fractional Na+ and Cl- excretions were higher during untreated than during CPAP-treated nights. 4. No difference in plasma active renin concentration or in urinary excretion of noradrenaline, adrenaline, free dopamine and total dopamine could be demonstrated, but cyclic GMP excretion was significantly higher during untreated than during CPAP-treated nights. 5. The data are consistent with the hypothesis that the increased water and salt excretion in OSA patients is due to increased ANF release. 6. The proposed mechanism is an atrial distension due to increased (more negative) intrathoracic pressures during ineffective inspiratory efforts against the occluded upper airways which have been found in OSA.
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PMID:Urinary excretion of guanosine 3':5'-cyclic monophosphate during sleep in obstructive sleep apnoea patients with and without nasal continuous positive airway pressure treatment. 253 3

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

We studied ten men with olivopontocerebellar degeneration. Our findings of the autonomic deficits as manifested by orthostatic hypotension, impaired Valsalva's response, abnormal findings on cold pressor and mental arithmetic tests, and plasma renin and norepinephrine abnormalities in some patients with olivopontocerebellar degeneration suggested a defective central control of the sympathetic nervous system. Five patients had sleep apnea. Autonomic dysfunction and sleep apnea in olivopontocerebellar degeneration may result from degenerative lesions in the cerebellum and the brain stem.
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PMID:Autonomic dysfunction and sleep apnea in olivopontocerebellar degeneration. 638 99

Polycythaemia, peripheral oedema formation and hypertension have classically been described in association with obstructive sleep apnoea (OSA). However, there is very limited information about blood volume in OSA and how it changes during long-term treatment with nasal continuous positive airway pressure (nCPAP). Plasma (PV) and red-cell volumes (RCV), 24-h ambulatory blood pressure (BP), 24-h natriuresis and morning plasma aldosterone, renin activity and atrial natriuretic peptide in 11 men with a mean age of 47 y (range 37-55), apnoea index (AI) of 55 (22-106), body mass index of 36 (30-43) and seated BP of > or = 140/90 mmHg without any medication were measured. BP-measurements were repeated after 3 weeks and all measurements after 3 mo of nCPAP treatment. Aldosterone and 24-h mean heart rates decreased during treatment. Twenty-four-h BP decreased after 3 weeks but that decrease did not persist after 3 mo of treatment. There was a relationship between changes in night-time mean BP and PV and aldosterone. The haematocrit declined in every patient. No significant changes were found in the mean PV or RCV. They were in all instances lower than has earlier been described for normal, non-obese subjects. These data also suggest that OSA causes divergent individual disturbances in blood volume homeostasis which can be corrected by nCPAP.
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PMID:Effect of nasal CPAP treatment on plasma volume, aldosterone and 24-h blood pressure in obstructive sleep apnoea. 895 8

Even if different mechanisms of various interactions during sleep are known, it is still unsolved by which mechanisms physiological reactions during sleep may start a pathophysiological course. Hypoxia, Hypercapnia and repetitive sympathetic elevations are well known elements in the control of the arterial resistance. Furthermore investigations in patients with sleep apnea showed changes of the pulsatile secretion pattern within the renin-angiotensin-system and the antinatriuretic peptides. These changes were reversible under nasal CPAP-therapy, nycturia as a frequent symptom disappeared. Nevertheless neither hypoxia nor intrathoracic pressure changes nor the arousals can assert the longterm influence on the blood pressure alone, a multifactorial confluence must be assumed. Further it is unclear how a tonic increase of the arterial blood pressure may occur in dependence of the REM- and NREM-sleep cycle changes as well as during daytime. First investigations in sleeping man seem to indicate, that a disturbance of the physiological coupling of breathing and circulation may present a pathogenetic element. Finally it remains open, whether the changes of the cardiorespiratory coupling during sleep of control persons and of patients with OSA are comparable, and whether they may be procured for an explanation of the pathogenesis of arterial and pulmonary hypertension. Further investigations in the control mechanisms of breathing and circulation related to the circuits of chemo- and baroreception, thresholds during wakefulness and sleep may be of decisive help to process the question, to what extent clinical states find a correlate in a disturbed cardiorespiratory coupling and, much more significantly, whether a disturbance in the physiological cardiorespiratory coupling appears already in early states of a disease. Sleep with ist complex physiology as well as with its characteristic pathophysiological phenomenon of sleep related breathing disorders has opened a new interdisciplinary field where tools like the polysomnography and electronic data analysis are used by physiologists, pathophysiologists as well as by physicians.
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PMID:[Cardiorespiratory coupling in obstructive sleep apnea (OSA)]. 924 90

A less-than-normal decline in nocturnal blood pressure (BP) has been associated with excessive hypertensive complications. This is concerning because secondary hypertension is often associated with this so-called nondipper BP profile. A nondipping pattern is more frequently found in the presence of pheochromocytoma, Cushing's syndrome, and sleep apnea syndrome, but the prevalence is unclear in patients with primary hyperaldosteronism. We therefore studied ambulatory BP profiles in 16 hypertensive patients with primary hyperaldosteronism and an equal number of essential hypertensive subjects. The awake-sleep BP difference of the hyperaldosteronism patients was similar to that of essential hypertensives (15/14 +/- 3/2 versus 14/9 +/- 3/2 mm Hg, P=NS). The prevalence of dippers and nondippers (according to two distinct criteria) in the two groups was similar. Repeat ambulatory BP monitoring in 12 subjects with primary hyperaldosteronism after specific intervention (3 after surgical removal of an adrenal adenoma and 9 after commencement and titration of spironolactone therapy) showed highly significant reductions in office BP (22/10 +/- 6/4 mm Hg, P<.05) and awake and sleep BP. However, the extent of nocturnal BP decline was unchanged between the two studies (17/16 +/- 3/3 versus 16/12 +/- 2/2 mm Hg, P=NS). There was no correlation between the awake-sleep difference and serum or urinary aldosterone levels or the aldosterone-to-renin ratio. In this study, we did not detect any differences in the awake-sleep differences between a group of hypertensives with primary hyperaldosteronism and a control group of essential hypertensives.
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PMID:Circadian blood pressure variation in hypertensive patients with primary hyperaldosteronism. 949 70

Previous studies in several strains of rats have demonstrated that 35 days of recurrent episodic hypoxia (EH) (7 hours per day), with a fractional concentration of inspired oxygen that produces desaturation equivalent to the recurrent hypoxemia of sleep apnea, results in an 8 to 13 mm Hg persistent increase in diurnal systemic blood pressure (BP). Carotid chemoreceptors and the sympathetic nervous system have been shown to be necessary for development of this BP increase. Both renal artery denervation and adrenal demedullation block the BP response to chronic EH. The present study was undertaken to define further the role of the kidneys and the renin-angiotensin system in this BP increase. Separate groups of male Sprague-Dawley rats had either (1) bilateral renal artery denervation with EH, (2) sham surgery with EH, (3) sham surgery with sham EH (compressed air), (4) EH with losartan, (5) unhandled with losartan, or (6) unhandled. The experimental period lasted 35 days. Both renal-artery denervated and losartan-treated animals showed no BP change or a lowering of BP in response to EH, whereas the sham-operated EH animals showed a progressive, sustained increase in resting room air BP. BP remained at basal levels or fell in unhandled and unhandled losartan-treated animals. Plasma renin activity was elevated 4-fold versus basal levels in EH animals with renal nerves intact but remained at baseline levels in denervated animals. At the end of the experiment, renal tissue catecholamines confirmed renal denervation in those animals. In conclusion, EH causes a progressive increase in BP, mediated in part through renal sympathetic nerve activity that acts to increase renin-angiotensin system activity through angiotensin II type 1 receptors.
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PMID:Renin activity and blood pressure in response to chronic episodic hypoxia. 1045 59

The evidence that plasma volume is altered in obstructive sleep apnoea is an indirect one, based on the observation of a paradoxical elimination of peripheral oedema along with a decrease in water and sodium excretion and of a decrease in haematocrit when apnoeas are eliminated with continuous positive airway pressure (CPAP) treatment. A suggested interpretation of these observations is that in the untreated condition, increased renal sodium excretion and increased vascular membrane permeability lead to increased urine and salt excretion and to a fluid shift from the plasma to the extracellular space, causing nocturnal polyuria, peripheral oedema and haemoconcentration. Treatment with continuous positive airway pressure reverses the increased membrane permeability and urine excretion, allowing the peripheral oedema to resolve and the haematocrit to decrease. Increased atrial natriuretic peptide release and decreased renin-angiotensin-aldosterone activity, along with an increased release of thromboxane and of endothelin (which have been reported in untreated obstructive sleep apnoea), could be the mechanisms of the observed alterations in fluid distribution in obstructive sleep apnoea.
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PMID:Regulation of plasma volume during obstructive sleep apnoea. 1060 85


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