atrial-natriuretic-factor and Sleep-Apnea-Syndromes

A number of pathophysiological phenomena linked to sleep disordered breathing are likely to affect vascular function. This report briefly reviews current knowledge regarding neurogenic vascular tone and a number of circulating hormones with vascular actions in obstructive sleep apnea (OSA). New evidence suggesting a role of the vascular endothelium in the development of vascular disease in OSA is also presented.

Topics: Aldosterone; Angiotensin II; Arginine; Atrial Natriuretic Factor; Endothelium; Humans; Hypertension; Sleep Apnea Syndromes; Snoring; Sympathetic Nervous System

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)

Topics: Atrial Natriuretic Factor; Blood Proteins; Cardenolides; Digoxin; Diuresis; Homeostasis; Humans; Kidney; Natriuresis; Plasma Volume; Renin; Saponins; Sleep Apnea Syndromes; Sodium-Potassium-Exchanging ATPase

Because sleep apnoea syndrome is often associated with arterial hypertension, it has been suggested that sleep apnoea might be responsible for hypertension. This hypothesis is mainly based on epidemiological studies showing a statistically significant association between snoring and arterial hypertension; this association remains true even after data correction to take into account the increased frequency of snoring with age and overweight. However, this statistical link is no evidence of a cause-effect relationship, and the mechanism through which sleep apnoea syndrome could produce arterial hypertension remains unknown. Yet treatment of sleep apnoea syndrome seems to improve arterial hypertension, and this alone would justify a search for sleep apnoea syndrome in all patients presenting with arterial hypertension.

Topics: Atrial Natriuretic Factor; Catecholamines; Humans; Hypertension; Positive-Pressure Respiration; Prevalence; Protriptyline; Sleep Apnea Syndromes; Tracheotomy

Patients with the sleep apnoea/hypopnoea syndrome have increased salt and water excretion at night which has been reported to be associated with an increase in plasma levels of atrial natriuretic peptide (ANP). A study was performed to determine whether any rise in plasma ANP levels was related to nocturnal hypoxaemia.. Nine patients with sleep apnoea/hypopnoea syndrome were studied on two nights, one breathing air and the other 28% oxygen, the order being randomised. Venous levels of ANP, aldosterone, and renin activity were measured.. No decrease in plasma ANP levels on oxygen was seen, and, indeed, there was no evidence of an overnight increase in ANP levels.. Oxygen therapy does not diminish nocturnal plasma ANP levels in patients with sleep apnoea/hypopnoea syndrome.

Topics: Aldosterone; Atrial Natriuretic Factor; Humans; Male; Middle Aged; Oxygen Inhalation Therapy; Random Allocation; Renin; Sleep Apnea Syndromes

1. Patients with obstructive sleep apnoea have increased diuresis during sleep, which decreases with nasal continuous positive airway pressure treatment. These changes have been attributed to an increased release of atrial natriuretic peptide in obstructive sleep apnoea, and its decrease with continuous positive airway pressure treatment. 2. In order to clarify the change in plasma atrial natriuretic peptide level and to investigate the underlying mechanisms, blood samples were taken at 10 min intervals from nine patients with obstructive sleep apnoea during two nights when the patients were either untreated or treated with continuous positive airway pressure. Polysomnographic monitoring, including transcutaneous oximetry, and measurement of oesophageal pressure were performed simultaneously. Plasma arginine vasopressin was also measured. 3. The plasma level of arginine vasopressin did not change. The level of atrial natriuretic peptide was high and exhibited secretion bursts in six out of the nine patients; it drastically decreased with continuous positive airway pressure treatment. 4. Across the patients, the mean plasma levels of atrial natriuretic peptide was correlated with the degree of hypoxaemia and the degree of oesophageal pressure swings during the sleep apnoeas. 5. Within the patients, cross-correlation studies suggested that the atrial natriuretic peptide secretory bursts were related either to the oesophageal pressure swings or to the apnoea-related hypoxaemia. 6. We conclude that release of atrial natriuretic peptide decreases with continuous positive airway pressure treatment in those patients with obstructive sleep apnoea who have increased release of atrial natriuretic peptide before treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Humans; Hypoxia; Positive-Pressure Respiration; Sleep Apnea Syndromes; Sodium

There is a close relationship between sleep disordered breathing (SDB) and heart failure. We performed home oxygen therapy (HOT) in patients with SAS undergoing dialysis, and investigated its effects on the heart function. The subjects were 10 SDB patients on dialysis. On retiring at night, oxygen was transnasally administered at 1.0 L/min. The human atrial natriuretic peptide (hANP), brain natriuretic peptide (BNP), total protein, Alb, cholesterol and phosphorus levels were measured before the start of oxygen therapy and after 6 weeks. The mean SpO2 increased from 93.5% [91.5, 97.0] to 96.3% [94.8, 97.4] (median [interquartile range]) (p = 0.015). The hANP (p = 0.0039), BNP (p = 0.0098) and serum Alb (p = 0.015) levels significantly improved. There were no significant changes in the cholesterol, phosphorus or total protein levels. These results suggest that nocturnal oxygen therapy improves indices of heart failure, contributing to the prevention and treatment of heart failure in dialysis patients with SDB.

Topics: Aged; Atrial Natriuretic Factor; Female; Heart Failure; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Oxygen; Quality of Life; Renal Dialysis; Sleep Apnea Syndromes

Topics: Adult; Aged; Asian People; Atrial Natriuretic Factor; Female; Humans; Japan; Male; Middle Aged; Risk Factors; Sleep Apnea Syndromes; Urban Population

Paroxysmal nocturnal dyspnea (PND) is a common symptom for patients with acute decompensated heart failure (ADHF). Some symptoms of PND are similar to those of sleep apnea (SA) which might be associated with overnight worsening hemodynamics in failing hearts. However, the association between PND, SA, and overnight change in hemodynamics in patients with heart failure remains uncertain.. We studied 28 consecutive patients with reduced ejection fraction who were hospitalized with ADHF. Plasma atrial natriuretic peptide (ANP) levels were measured before and after overnight sleep study. PND was defined as having an episode of PND prior to hospitalization for ADHF.. Ten (36%) patients had a history of PND. Respiratory disturbance index (the frequency and severity of sleep apnea) was an independent factor associated with a history of PND (odds ratio 1.24, 95% confidence interval 1.05-1.47, p=0.011). In those without PND, plasma ANP levels decreased from before sleep to after waking, whereas in those with PND it increased (p=0.011). In addition, overnight change in plasma ANP levels was independently associated with respiratory disturbance index (p=0.035).. These results thus suggest that in patients with ADHF, SA might be a predisposing cause of PND in association with overnight worsening hemodynamics.

Topics: Acute Disease; Atrial Natriuretic Factor; Dyspnea, Paroxysmal; Female; Heart Failure; Hemodynamics; Hospitalization; Humans; Male; Middle Aged; Sleep Apnea Syndromes

Topics: Atrial Natriuretic Factor; Cardiovascular Diseases; Chronic Disease; Circadian Rhythm; Comorbidity; Continuous Positive Airway Pressure; Heart Failure; Humans; Natriuretic Peptide, Brain; Oxygen; Polysomnography; Sleep Apnea Syndromes; Wakefulness

We compared brain natriuretic peptide (BNP) levels in patients with obstructive sleep apnea (OSA) with and without cardiovascular disease to BNP in healthy control subjects. OSA was not associated with increased plasma BNP or atrial natriuretic peptide (ANP) in otherwise healthy subjects during wakefulness. Untreated OSA increased ANP overnight, and ANP levels decreased with treatment of OSA. However, OSA did not elicit acute overnight changes in BNP, either in normal subjects or in patients with coexisting cardiovascular disease (including chronic heart failure).

Topics: Adult; Aged; Atrial Natriuretic Factor; Cardiovascular Diseases; Chronic Disease; Circadian Rhythm; Comorbidity; Continuous Positive Airway Pressure; Heart Failure; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Oxygen; Polysomnography; Reference Values; Sleep Apnea Syndromes; Wakefulness

To assess the utility of urinary uric acid excretion and urinary uric acid/creatinine ratio as the marker of nocturnal respiratory disturbance in patient with sleep apnea syndrome (SAS) before and after the institution of nasal continuous positive airway pressure (nCPAP). Another purpose is to explore the relationship between the nocturnal diuresis and atrial natriuretic peptide (ANP), renin-aldosterone in SAS.. 22 cases diagnosed as SAS by polysomnography (PSG) were selected as trial group, 11 cases excluded from SAS by PSG were as control group, and 13 severe SAS patients were treated by nCPAP and taken as nCPAP therapy group. The markers mentioned above were compared in these groups.. The overnight change in urinary uric acid/creatinine ratio in trial group is 0.47 +/- 0.31, which is significantly higher than that in control group (0.01 +/- 0.23), P < 0.05, and in nCPAP therapy group after therapy (0.01 +/- 0.19) significantly lower than that before nCPAP therapy (0.48 +/- 0.27), P < 0.001. The morning urinary uric acid excretion in trial group is (5.4 +/- 2.3) mg/L which is also significantly higher than that in control group (3.2 +/- 1.4) mg/L, P < 0.001, and in nCPAP therapy group (3.3 +/- 1.2) mg/L significantly lower than that before nCPAP (5.9 +/- 2.6) mg/L, P < 0.05. The mean morning blood ANP in trial group is (0.182 +/- 0.004) microgram/L, which is higher than that in control group (0.182 +/- 0.004) microgram/L, P < 0.05, and in nCPAP therapy group (0.122 +/- 0.001) microgram/L is much lower than that before nCPAP therapy (0.180 +/- 0.003) microgram/L, P < 0.001. However there are no statistic significant differences between these groups in blood renin-aldosterone.. The urinary uric acid excretion and overnight change in urinary uric acid/creatinine are good markers to determine the effects of nCPAP on SAS. The nocturnal diuresis in SAS patients is correlated with the increase of ANP in plasma.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Creatinine; Female; Humans; Male; Middle Aged; Renin; Sleep Apnea Syndromes; Uric Acid

Elevated nocturnal plasma atrial natriuretic peptide (ANP) levels were found in patients with obstructive sleep apnoea (OSA). The purpose of our study was to examine the secretion of ANP during the night and to measure changes in oxygen saturation, pulmonary artery pressure and intrathoracic pressure swings in patients with OSA. Moreover, we analysed the secretion of ANP and the pulmonary artery pressure in different behavioural states, e.g. awake, at exercise and asleep. Consecutive apnoeas in non-rapid eye movement (NREM) sleep at the beginning, middle and end of the sleep study were analysed in six patients with obstructive sleep apnoea. In addition, we measured the plasma levels of ANP. The apnoea duration was significantly longer (P< 0.05) at the middle of the sleep study than at the beginning or end. Correspondingly, the end-apnoeic oxygen saturation and end-apnoeic oesophageal pressure were both significantly lower (P< 0.05) in the middle of the sleep study than at the beginning or end. No significant differences were found in the end-apnoeic systolic transmural pulmonary artery pressure (P(PATM)) and the levels of ANP. Evaluation of the ANP levels during different behavioural states revealed that the asleep levels were slightly, but not significantly, higher than the awake levels (0.235+/-0.088 vs. 0.207+/-0.057 nmol/L). However, the highest levels were found during exercise (0.334+/-0.170 nmol/L) with a significant difference compared with the awake and asleep levels. These data suggest that volume effects may be a potent factor in liberating ANP during exercise, but the role of OSA in ANP secretion when asleep is questionable.

Topics: Atrial Natriuretic Factor; Body Mass Index; Exercise; Hemodynamics; Humans; Male; Middle Aged; Polysomnography; Pulmonary Wedge Pressure; Severity of Illness Index; Sleep Apnea Syndromes; Sleep, REM; Wakefulness

The nocturnal secretion profile of the newly identified natriuretic peptide (NP), brain natriuretic peptide (BNP), was studied in 14 patients with obstructive sleep apnoea syndrome (OSAS) (apnoea hypopnoea index: 60.5 +/- 3.4, mean +/- SE) during two separate nights before and during nasal continuous positive airway pressure (NCPAP) therapy. Plasma levels of NPs (atrial natriuretic peptides; ANP and BNP) were measured at 2-h intervals during sleep. Simultaneously, blood pressure was measured by a non-invasive method (Finapres, Ohmeda, Englewood, CO, USA) and urine was collected for determining volume and catecholamine levels. Urinary and serum sodium concentration were determined before and after the study. Eight non-snoring subjects were also studied for the investigation of normal nocturnal profiles of BNP levels. To understand the discrete secretion profiles of the two NPs during sleep, blood was sampled from an additional seven patients every 5 min over a 30-min period around 00.00 and 04.00 hours before NCPAP. In patients with OSAS, plasma BNP levels increased from the beginning of sleep (22:00 h) to the morning (06:00 h) before NCPAP therapy (P < 0.01, ANOVA). Baseline BNP levels were not significantly correlated with patient's clinical and polysomnographic parameters. However, in the latter half of the sleep period (02:00-06:00 h), increases in BNP levels during the night before NCPAP therapy were significantly correlated with blood pressure elevations (systolic: r = 0.784 P < 0.01, diastolic: r = 0.587 P < 0.01) and with apnoea duration (r = 0.582 P < 0.01). In normal subjects BP and BNP levels were not changed significantly during sleep. Plasma BNP levels were well correlated with concomitant ANP levels (P < 0.001). NCPAP therapy reduced ANP and BNP levels during sleep and in the morning (P < 0.01). Plasma levels of BNP at 5 min intervals before NCPAP therapy revealed few variations. On the other hand, ANP levels fluctuated over the 30-min period. Changes in BNP levels during sleep in the patients with OSAS may be related to blood pressure variations, but may be too small to play a significant physiological role in regulating diuresis in OSAS. Further work is required to determine the precise role of dual natriuretic system in cardiovascular load and natriuresis in OSAS.

Topics: Atrial Natriuretic Factor; Blood Pressure; Circadian Rhythm; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Polysomnography; Positive-Pressure Respiration; Severity of Illness Index; Sleep Apnea Syndromes

Seven normotensive untreated patients with obstructive sleep apnea (OSA) and five control subjects without OSA were compared. Patients with cardiac dilation, chronic airflow limitation, liver and kidney disease, or diabetes mellitus were excluded. Change in pressure-heart rate relation to alpha-adrenergic stimulation (P-HRR), extracellular volume (ECV), and plasma volume (Vp) were measured during daytime. Plasma atrial natriuretic peptide (ANP), plasma renin and aldosterone concentrations were obtained at 1 hour intervals during the night. A mean apnea/hypopnea index (AHI) of 52.2 +/- 23.9/h and a mean lowest arterial oxygen saturation (SaO2) of 61.2 +/- 19.3% (mean +/- SD) were determined from polysomnographic monitoring in the patient group. Release of ANP was significantly higher during sleep in OSA patients than in control subjects (P < .01), with a maximum concentration between 4 and 6 AM in the former. Daytime ECV was significantly higher (P < .05) and Vp significantly lower (P < .05) in OSA patients. Night maximum concentration of ANP (max ANP) was negatively related to AHI (P < .05). P-HRR was negatively related to AHI (P < .05) and positively related to max ANP (P < .05). In conclusion, OSA syndrome alters hormonal system control of body fluid compartment regulation. The decreased response in night max ANP secretion in the most severe OSA patients could be explained by the smaller Vp observed in these patients, decreasing atrial and ventricular pressure loading. Furthermore, alteration of P-HRR, correlated to AHI and max ANP, strengthens the hypothesis that patients who develop hypertension are those in whom the protective mechanism of ANP release failed.

Topics: Adrenergic alpha-Agonists; Adult; Aldosterone; Atrial Natriuretic Factor; Blood Pressure; Heart Rate; Humans; Middle Aged; Renin; Sleep Apnea Syndromes

Elevated plasma atrial natriuretic peptide (ANP) levels and concomitant increases in renal sodium and water excretion are often encountered in respiratory diseases associated with increased airway resistance such as obstructive sleep apnea. The present study utilized an anesthetized rat model to determine the principal mechanism(s) responsible for stimulation of ANP release in this clinical syndrome. A 10-minute increase in external resistive loading, which reduced peak tracheal pressure to -15 to -17 mm Hg produced a significant increase in both central venous pressure and right atrial transmural pressure. This maneuver subsequently resulted in significant transient increases in glomerular filtration rate; urine flow; urinary Na+, K+, and Cl- excretion; and urinary cyclic guanosine monophosphate (cGMP) excretion, which was taken as an index of increased circulating levels of ANP. Similar changes in renal function and cGMP excretion occurred when arterial PO2 was lowered to a degree equivalent to that seen with increased resistive loading. Lowering arterial PO2 also significantly increased mean central venous pressure and right atrial transmural pressure. Conversely, the resistive loading-induced changes in renal function and cGMP excretion did not occur when the reduction in arterial PO2 was prevented by breathing a high O2 gas mixture during the resistive loading. Additionally, O2 supplementation prevented the increases in both mean central venous pressure and right atrial transmural pressure caused by increased resistive loading. These data indicate that the elevated ANP release that results from an acute increase in external resistive loading is not caused by a decrease in intrathoracic pressure but rather suggest that the elevated ANP release is primarily caused by an increased right atrial transmural pressure resulting from hypoxia-induced pulmonary vasoconstriction.

Topics: Airway Resistance; Animals; Atrial Natriuretic Factor; Disease Models, Animal; Heart; Hypoxia; Kidney Function Tests; Lung; Male; Oxygen; Partial Pressure; Rats; Rats, Sprague-Dawley; Sleep Apnea Syndromes; Vasoconstriction

Topics: Aldosterone; Atrial Natriuretic Factor; Body Water; Guanosine Monophosphate; Hemodynamics; Humans; Positive-Pressure Respiration; Renin; Sleep Apnea Syndromes; Sodium; Vasopressins

The relationship between airway obstruction during sleep and changes in mean arterial pressure (MAP) was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. The MAP response was determined 1) during experimental airway obstruction whenever sleep occurred, 2) over each 12-h experiment, and 3) during a 2-h recovery period at the end of each experiment. The effects of 24 h of sleep deprivation and changes in plasma levels of renin and atrial natriuretic peptide were assessed. In non-rapid-eye-movement sleep, a period of airway obstruction caused MAP to increase (P < 0.002) from 95 +/- 3 (SE) mmHg to 112 +/- 3 mmHg, and this difference was enhanced (P < 0.04) by sleep deprivation. There was an increase of 12 +/- 2 mmHg in the overall MAP over time (P < 0.001) in non-rapid-eye-movement sleep that was sustained in the 2-h recovery period. Plasma levels of renin and atrial natriuretic peptide were constant and unrelated to changes in MAP. We conclude that in the sleeping dog airway obstruction causes an increase in MAP that can be accentuated by prior sleep deprivation and that repetitive airway obstruction will cause an increase in MAP over time that is sustained for > or = 2 h when normal airway patency is restored.

Topics: Airway Obstruction; Animals; Atrial Natriuretic Factor; Blood Pressure; Circadian Rhythm; Dogs; Electrocardiography; Female; Hydrocortisone; Male; Polysomnography; Radioimmunoassay; Renin; Sleep; Sleep Apnea Syndromes; Tracheostomy

To evaluate atrial natriuretic factor (ANF) secretion during sleep in obstructive sleep apnea syndrome (OSAS), plasma ANF was measured every 3 hours before and after effective nasal continuous positive airway pressure (CPAP) treatment in 10 patients with moderate to severe OSAS and 10 normal subjects. The results showed daily changes in ANF levels in normal controls and in OSAS patients after effective therapy, with a nadir at 0300 hours and a peak at 2100 hours. There was no significant daily variation of ANF levels in patients with OSAS before therapy, and ANF levels from midnight to 0900 hours were significantly higher before, as compared with after, therapy. These results indicate that OSAS patients have abnormal ANF secretion. Effective nasal CPAP therapy led to normalization of ANF secretion during sleep.

Topics: Adult; Analysis of Variance; Atrial Natriuretic Factor; Circadian Rhythm; Female; Humans; Male; Positive-Pressure Respiration; Radioimmunoassay; Sleep Apnea Syndromes

Patients with obstructive sleep apnea (OSA) syndrome are known to exhibit nocturnal natriuresis/diuresis. We studied plasma and urinary levels of atrial natriuretic peptide (ANP), a potent natriuretic hormone released from the heart, and plasma antidiuretic hormone (ADH) levels in patients with OSA during awake and sleeping periods, to compare with those of normal subjects. Seven patients with OSA and 6 normal subjects were studied. Arterial blood samples were drawn during the awake and the sleeping period, while in patients with OSA, blood samples were obtained during the apneic period. Urine samples were collected over two 12-hour periods (9 a.m.-9 p.m. and 9 p.m.-9 a.m.) In patients with OSA, plasma ANP as well as urinary ANP excretion increased during the apneic period compared with the awake period. There was a significant negative correlation between plasma levels of ANP and ADH in patients with OSA. On the other hand, normal subjects had no apparent differences in plasma and urinary ANP levels between the two periods. It is suggested that nocturnal increase in ANP and decrease in ADH are responsible for the nocturnal diuresis and natriuresis associated with OSA.

Topics: Adult; Atrial Natriuretic Factor; Case-Control Studies; Circadian Rhythm; Diuresis; Female; Humans; Male; Middle Aged; Sleep; Sleep Apnea Syndromes; Vasopressins

In ten patients with severe obstructive sleep apnea (OSA) profound changes in renal function could be demonstrated at night during nCPAP therapy. Natriuresis and diuresis decreased by about 50% while creatinine excretion rate and urinary osmolality did not change. We found parallel changes in the excretion of ANP's second messenger cyclic guanosine monophosphate (cGMP) in a dose-response-related manner to natriuresis respectively diuresis. These data are in agreement with recently demonstrated decrease of nocturnal plasma levels of atrial natriuretic peptide (ANP) during nCPAP therapy in apneic patients. This may be an indicator for an increased cardiac volume load during obstructive apnea. The decrease of diuresis, natriuresis and cGMP excretion demonstrate the beneficial effects of nCPAP treatment on the cardiovascular system. Therefore measurements of cGMP excretion may be a useful parameter to assess the cardiovascular function of apneic patients before and during treatment.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Circadian Rhythm; Cyclic GMP; Diuresis; Female; Humans; Male; Middle Aged; Natriuresis; Positive-Pressure Respiration; Second Messenger Systems; Sleep Apnea Syndromes

We studied nocturnal and early morning variations in the concentration of plasma atrial natriuretic peptide (ANP) in 17 men who habitually snored. The subjects had a mean age of 51.0 +/- 5.8 years, range 41-62 y with a mean body mass index (BMI) of 32.9 +/- 7.3 kg/m2. The concentration of plasma ANP was measured by radioimmunoassay of venous samples at 10 p.m., midnight, 6 p.m. and 8 p.m. All night sleep recordings were conducted with the static charge sensitive bed to monitor body and breathing movements and a BIOX III Pulse Oximeter for the blood oxygen saturation level. Nine patients were defined as having the obstructive sleep apnea syndrome (OSAS). No significant diurnal variation for ANP concentrations was detected. At 8 a.m. five OSAS patients and two others had ANP concentrations above normal (70 pg/ml). Neither mean oxygen saturation during the night nor arterial hypertension discriminated between the high and low ANP groups at 8 a.m. The best discriminators for a high concentration of ANP at 8 p.m. were marked obesity (BMI greater than or equal to 30 kg/m2), over 400 movements lasting less than five seconds, and over 30% of active sleep per night. In a multivariate regression analysis age, percentage of active sleep during the night, BMI and the median oxygen saturation level during the night explained 76.4% of the total variance of ANP at 8 a.m. In a similar analysis the median oxygen saturation level during the night and BMI both explained the variance of ANP significantly. The whole model explained 53.7% of the variance of the ANP concentrations at 6 a.m.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Atrial Natriuretic Factor; Body Mass Index; Circadian Rhythm; Humans; Male; Middle Aged; Oxygen; Sleep Apnea Syndromes; Snoring

Topics: Atrial Natriuretic Factor; Circadian Rhythm; Humans; Oxygen; Positive-Pressure Respiration; Renin; Sleep Apnea Syndromes; Water-Electrolyte Balance

Nocturnal polyuria with repeated micturitions during the night is a clinically evident feature of obstructive sleep apnea syndrome (OSAS). These effects are reversed by continuous positive airway pressure (CPAP). There is some evidence that atrial natriuretic peptide (ANP) and catecholaminergic activity may be implicated in the pathogenesis of these symptoms. We studied these biochemical parameters in six patients with severe OSAS during two nights: the first (basal) in their normal conditions and the second during CPAP treatment. CPAP treatment reversed apnea episodes in all our patients. A significant (p less than 0.035) reduction of nocturnal urine volume (from 902 +/- 297 to 447 +/- 130 ml; mean +/- SD), sodium excretion (from 150 +/- 33 to 89 +/- 35 mEq/12 h), noradrenaline excretion (from 95 +/- 101 to 52 +/- 16 micrograms/g creatinine), noradrenaline plasma concentrations (from 325 +/- 96 to 259 +/- 75 pg/ml), ANP plasma concentrations (from 35 +/- 20 to 19 +/- 5 pg/ml) was observed during the night under CPAP application. These data suggest that in OSAS patients the high ANP plasma concentration is responsible for the observed elevated diuresis and sodium excretion. These effects are rapidly reversible, as they are reversed during the first CPAP treated night.

Topics: Adult; Atrial Natriuretic Factor; Epinephrine; Humans; Male; Middle Aged; Norepinephrine; Oxygen; Positive-Pressure Respiration; Sleep Apnea Syndromes; Sleep Stages

1. Plasma levels of atrial natriuretic peptide (ANP) were measured in seven patients with obstructive sleep apnoea (OSA) while they were awake, during repetitive apnoea and during treatment with nasal continuous positive airway pressure (CPAP). 2. ANP levels in both pulmonary artery and peripheral venous samples were elevated during apnoeic sleep and reduced when apnoea was prevented by nasal CPAP. Mean values of pulmonary artery ANP were 116.3 +/- 17.9 pg/ml during apnoea and 64.8 +/- 15.2 pg/ml (P less than 0.05) on nasal CPAP. 3. It is concluded that there is increased ANP release during sleep in patients with OSA and that CPAP treatment normalizes ANP secretion. These findings may explain previously identified urinary abnormalities in OSA.

Topics: Atrial Natriuretic Factor; Humans; Male; Nose; Positive-Pressure Respiration; Sleep Apnea Syndromes

It has long been known that the heart is involved volume regulation. This fact took on new importance when, in 1981, de Bold discovered the existence of ANF. Apnea-associated cardiovascular changes make the treatment of apnea necessary to prevent the occurrence of cardiovascular sequelae. What is needed, however, is a parameter which, non-invasively, reflects both the cardiac loading during apnea and effects of treatment. Krieger succeeded in demonstrating that the commonly observed nycturia regresses under nasal cPAP therapy. This prompted us to consider whether the ANF factor might not be involved. In an attempt to find an answer, we have, up to now, investigated six patients prior to and during nCPAP therapy. On the basis of the results we obtained, the following conclusions may be drawn: 1. During apnea, the patients show sometimes dramatic increases in ANF plasma levels. 2. Under nasal CPAP treatment, these elevated levels decrease again, in some cases by as much as 50%. 3. The ANF plasma level correlates with pulmonary arterial pressure. This suggests to us that ANF determination is of importance for the assessment of cardiac loading during apnea, and represents a parameter that reflects the effects of therapy.

Topics: Atrial Natriuretic Factor; Humans; Hypertension, Pulmonary; Middle Aged; Pulmonary Heart Disease; Pulmonary Wedge Pressure; Risk Factors; Sleep Apnea Syndromes

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.

Topics: Adult; Aged; Atrial Natriuretic Factor; Chlorides; Cyclic GMP; Female; Humans; Kidney; Male; Middle Aged; Positive-Pressure Respiration; Renin; Renin-Angiotensin System; Sleep Apnea Syndromes; Sodium; Water