atrial-natriuretic-factor and Sleep-Apnea--Obstructive

Topics: Atrial Natriuretic Factor; Cost-Benefit Analysis; Disease Progression; Humans; Kidney Failure, Chronic; Kidney Transplantation; Natriuretic Peptide, Brain; Oximetry; Polysomnography; Positive-Pressure Respiration; Sleep Apnea, Obstructive; Sleep Stages; Treatment Outcome

Intermittent hypoxia stimulates the development of adaptive responses, called preconditioning. This process is partially mediated by genetic remodeling, via hypoxia inducible factor (HIF), which induces long-term adaptation processes and is responsible for the increase of levels of vascular endothelial growth factor (VEGF), erythropoietin (Epo), atrial natriuretic peptide (ANP), and nitric oxide (NO). The synthesis of brain-derived neurotrophic factor (BDNF) participates in the control of neural plasticity after hypoxia. The mechanisms of neuroprotection against hypoxia may be related to vascular adjustments and to central neurogenic neuroprotection. Some of the factors known to be involved in the development of the mechanism of neuroprotection are also present in the responses to repetitive apneas that occur during sleep in patients with obstructive sleep apnea (OSA) syndrome, who are frequently exposed to severe sleep hypoxemia. It appears that OSA syndrome represents a clinical example of preconditioning and the development of adaptive responses to intermittent hypoxia.

Topics: Adaptation, Biological; Animals; Atrial Natriuretic Factor; Brain-Derived Neurotrophic Factor; Erythropoietin; Humans; Nitric Oxide; Sleep Apnea, Obstructive; Vascular Endothelial Growth Factor A

Sleep-disordered breathing (SDB), including Cheyne-Stokes respiration with central sleep apnea (CSR-CSA), causes a deterioration in the prognosis of patients with chronic heart failure (CHF). Adaptive servo-ventilation (ASV) and oxygen therapy (O(2)) are useful for improving the CSR-CSA of CHF. The purpose of the present study was to examine the short-term effects of ASV and O(2) on suppressing SDB (CSR-CSA dominant) in CHF, and the accompanying neurohumoral abnormalities (cardiac overload, sympathetic nervous activation, and myocardial damage).. FORTY-two patients with CHF and SDB (mean LVEF 34.6%, apnea hypopnea index (AHI) 39.0/h, central apnea index (CAI) 17.6/h, obstructive apnea index (OAI) 2.6/h) were enrolled. We performed polysomnography (baseline, O(2), and ASV) for 3 consecutive days, and we measured levels of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), noradrenalin, urinary catecholamines, and high-sensitivity troponin T. Both O(2) and ASV reduced the AHI, CAI, arousal index, mean heart rate during sleep, and the levels of noradrenalin, urinary catecholamines, and high-sensitivity troponin T. However, only ASV, not O(2), decreased the levels of ANP and BNP.. ASV reduces cardiac overload, attenuates sympathetic nervous activity and ongoing myocardial damage effectively in CHF patients with SDB, and for patients who cannot use ASV, O(2) is an alternative therapy.

Topics: Aged; Atrial Natriuretic Factor; Chronic Disease; Cross-Over Studies; Female; Heart Failure; Humans; Male; Middle Aged; Myocardium; Oxygen; Sleep Apnea, Obstructive; Sympathetic Nervous System; Troponin T

Hypertension occurred in 50% obstructive sleep apnea-hypopnea syndrome (OSAHS) patients meanwhile OSAHS occurred in 30% hypertension patients. The present study aimed to explore the molecular mechanism of GATA2-EDN1-AGT induced hypertension in the development of obstructive sleep apnea-hypopnea syndrome. OSAHS patients (56 cases: 36 cases of male, 20 cases of female, 42~60 years old) were divided into two groups (case group: patients with hypertension monitored by 24 h ambulatory blood pressure and polysomnography; control group: patients without hypertension). Wistar rats were used to establish the OSAHS model (narrow pharyngeal cavity). PaO2 and PaCO2 of patients and rats were measured by an automatic blood gas analyzer. The profile of total protein in the OSAHS group and normal group was evaluated. Protein-protein-interaction (PPI) was carried out to show all matter proteins related. The levels of EDN-1, AGTII and atrial natriuretic peptide (ANP) in blood samples of patients and rats were analyzed by enzyme-linked immunosorbent assay (ELISA). The expression of GATA2, EDN1, endothelin-converting enzyme 1 (ECE-1) and AGTⅡ was measured. The results showed that SaO2 and AHI were positively associated with systolic pressure (P<0.05) in OSAHS patients. There was no correlation among other indexes (P>0.05). It was also observed that GATA2 had a strong relationship with AGTⅡ and EDN1. The results of ELISA presented that the levels of EDN1, AGTⅡ and ANP in the OSAHS group of human and animal models were significantly increased (P<0.05). The results of immunochemistry showed that the expression of GATA2 and AGTⅡ in the vascular of OSAHS group was upregulated manifestly (P<0.05). It was concluded that OSAHS can induce AHI, which increases hypertension via the GATA2-EDN1-AGT Ⅱ axis.

Topics: Angiotensinogen; Animals; Atrial Natriuretic Factor; Blood Pressure Monitoring, Ambulatory; Endothelin-1; Female; GATA2 Transcription Factor; Hypertension; Male; Rats; Rats, Wistar; Sleep Apnea, Obstructive; Syndrome

Obstructive sleep apnea (OSA) might lead to oxidative stress, inflammation and elevated circulating copeptin, proANP and proADM levels. We aimed to evaluate whether the levels of these prohormones are higher in patients with OSA and whether they might change under continuous positive airway pressure (CPAP) therapy, serving as potential proxies for the diagnosis and therapy-response in OSA.. A total of 310 patients with suspicion of OSA were recruited. Screening for OSA was performed using overnight pulse oximetry followed by polygraphy and a venous puncture in the morning. All patients diagnosed with OSA underwent CPAP adaptation. A venous puncture was conducted in the night before CPAP and in the following morning. At 1 and 6 months of treatment, polygraphy was performed, followed by a venous puncture in the morning. In the acquired blood, copeptin, proANP and proADM levels were measured.. We analyzed 232 patients with OSA and 30 patients without OSA. Our results indicated that only copeptin levels differed significantly among patients with and without OSA at baseline. In OSA patients, the levels of proADM significantly changed after 1 and 6 months on CPAP therapy, when compared to baseline (p < 0.001 and p = 0.020). Additionally, proANP levels significantly decreased after 12 h on CPAP therapy, as compared to baseline levels (p < 0.001).. Copeptin is significantly associated with the presence of OSA. ProANP levels might serve as a potential proxy for the acute response to non-invasive ventilation (12 h), while proADM reflects the long-term response (1 and 6 months).

Topics: Adrenomedullin; Adult; Aged; Atrial Natriuretic Factor; Biomarkers; Continuous Positive Airway Pressure; Female; Glycopeptides; Humans; Hypoxia; Longitudinal Studies; Male; Middle Aged; Prospective Studies; Protein Precursors; Sleep Apnea, Obstructive; Time Factors; Treatment Outcome; Up-Regulation

To investigate the urodynamic changes in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and nocturnal polyuria.. From Sept. 2002 to Jun. 2008, 23 patients with nocturnal polyuria were diagnosed as having OSAHS by polysomnography (PSG). The number and output of nocturia, the osmotic pressure and the excretion of Na(+) were recorded during both the PSG night and CPAP titrating night. Plasma levels of brain natriuretic peptide (BNP) and atrial natriuretic peptides (ANP) were also measured at 11PM in the 2 nights and 7AM in the next mornings. Urodynamic studies including urine flow, bladder pressure during filling, pressure-flow study during voiding and urethral pressure were carried out in these patients. Urodynamic studies were performed again after treatment with CPAP for 3 months.. PSG showed that the patients with nocturnal polyuria had moderate to severe OSAHS, in which the apnea-hypopnea index (AHI) being 48 ± 15 events per hour. The number of nocturnal voiding during the PSG night was more than that during the CPAP titrating night. During the PSG night, the output of nocturia, the nocturia excretion of Na(+), ANP levels (at 7am in the next morning after PSG night) increased and the osmotic pressure of nocturia decreased. CPAP therapy could reverse these abnormalities. The main characteristics of urodynamics in these patients included weak detrusor contraction, hypoesthesia in filling cystometry, and decreased bladder compliance, and detrusor external sphincter dyssynergia. After 3 months of CPAP treatment, both the motility of the detrusor of bladder and the bladder compliance improved.. CPAP therapy can effectively reverse the nocturnal polyuria in OSAHS patients. In OSAHS patients, the features of nocturia, including the changes of output, osmotic pressure and the excretion of Na(+), may be related to the secretion of high-level of ANP. During the course of chronic progressively OSAHS pathophysiology, detrusor function of bladder may be damaged. CPAP therapy could decrease the nocturnal excretion of ANP, and improve the motility of the detrusor of bladder.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Nocturia; Polyuria; Sleep Apnea, Obstructive; Urinary Bladder; Urodynamics

The cardiorenal syndromes (CRS) are composed of five recently defined syndromes which represent common clinical scenarios in which both the heart and the kidney are involved in a bidirectional injury process leading to dysfunction of both organs. Common to each subtype are multiple complex pathogenic factors, a precipitous decline in function and a progressive course. Most pathways that lead to CRS involve acute injury to organs which manifest evidence of chronic disease, suggesting reduced ability to sustain damage, maintain vital functions, and facilitate recovery. Prevention of CRS is an ideal clinical goal, because once initiated, CRS cannot be readily aborted, are not completely reversible, and are associated with serious consequences including hospitalization, complicated procedures, need for renal replacement therapy, and death. Principles of prevention include identification and amelioration of precipitating factors, optimal management of both chronic heart and kidney diseases, and future use of multimodality therapies for end-organ protection at the time of systemic injury. This paper will review the core concepts of prevention of CRS with practical applications to be considered in today's practice.

Topics: Anemia; Atrial Natriuretic Factor; Cardiotonic Agents; Dopamine; Heart Failure; Humans; Inflammation; Infusions, Intravenous; Kidney Diseases; Kidney Failure, Chronic; Myocardial Ischemia; Randomized Controlled Trials as Topic; Renal Circulation; Sleep Apnea, Obstructive; Sodium; Sodium Potassium Chloride Symporter Inhibitors; Syndrome

The mechanisms involved in the development and maintenance of hypertension in obstructive sleep apnoea (OSA) are not clear. We hypothesized that OSA patients have an abnormal renal handling of sodium and water during the night.. We studied 29 OSA patients and 19 healthy controls at night with serial determinations of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), arginine vasopressin (AVP), aldosterone (Aldo), fractional urinary excretion of sodium (FE(Na)), free water clearance (C(H2O)), urinary excretion of aquaporin 2 (u-AQP2), systolic blood pressure (SBP), diastolic blood pressure (DBP) and oxygen saturation.. OSA patients had a higher FE(Na) (0.6 (0.4-1.0) versus 0.4 (0.3-0.6) %; p = 0.017), SBP (129 (114-145) versus 114 (106-122) mmHg; p = 0.001) and DBP (81 (72-87) versus 71 (65-74) mmHg; p<0.001) than healthy controls at night. In hypertensive OSA patients, the FE(Na) correlated significantly with the change in nocturnal DBP (r (2) = 0.411; p = 0.010). Mean level of AVP during the night was higher in OSA patients compared with healthy controls (1.1 (0.8-1.4) versus 0.8 (0.6-1.1) pmol/L; p = 0.033) and correlated with SBP. ANP, BNP, Aldo, C(H2O) and u-AQP2 were the same in OSA and controls.. We conclude that the higher fractional excretion of sodium in OSA is most likely attributable to pressure natriuresis. The correlation between mean AVP and blood pressure suggests that AVP may be part of the pathogenetic mechanism underlying hypertension in these patients.

Topics: Adult; Age Factors; Aldosterone; Aquaporin 2; Arginine Vasopressin; Atrial Natriuretic Factor; Blood Pressure; Female; Humans; Hypertension; Kidney; Male; Middle Aged; Natriuresis; Natriuretic Peptide, Brain; Oxygen; Potassium; Sex Factors; Sleep Apnea, Obstructive; Sodium; Vasopressins; Water

Topics: Atrial Natriuretic Factor; Blood Pressure; Body Mass Index; Case-Control Studies; Diuresis; Humans; Kidney; Natriuretic Peptide, Brain; Sleep Apnea, Obstructive; Sodium

During obstructive sleep apneas stimuli, that may increase excretion of atrial natriuretic peptide (ANP) occur. The aim of the study was the evaluation whether in patients with OSAS levels of ANP are significantly different in relation to sleep or wakefulness and in relation to disturbances of ventilation during sleep and wakefulness. The material of the study consisted of 34 patients with OSAS (age 25-65 years). There were no differences in the levels of ANP late in the evening, during sleep and early in the morning. There were 2 groups of the patients: with low (< 70 pg/ml, mean at 21 p.m. 9.7 +/- 8.7 pg/ml, at. 2 a.m. 12.5 +/- 9.3 pg/ml, at 6 a.m. 14.4 +/- 15.1 pg/ml) and high (> 70 pg/ml, mean at 21 p.m. 148.6 +/- 232.9 pg/ml, at 2 a.m. 119.5 +/- 45.5 pg/ml, at 6 a.m. 164.9 +/- 161 pg/ml) ANP levels. As compared with patients with low ANP levels, patients with high ANP levels were older and more obese, more frequently had concomitant COPD, lower VC and FEV1, higher daytime PaCO2 and lower PaO2; most of them had peripheral edema. In patients with high ANP levels there was more profound mean arterial blood desaturation during sleep apnoeas than in patients with low ANP levels (SaO2 75 +/- 8% vs 81 +/- 4%, p < 0.001), although apnea index and mean apnea duration were similar in both groups.. In patients with OSAS the daytime and sleep levels of ANP are similar. High levels of ANP can be found in OSAS patients with impaired daytime ventilation and gas exchange, and profound arterial oxygen desaturation during sleep apnoeas.

Topics: Adult; Aged; Atrial Natriuretic Factor; Circadian Rhythm; Female; Forced Expiratory Volume; Humans; Male; Middle Aged; Oxygen; Pulmonary Gas Exchange; Sleep Apnea, Obstructive; Vital Capacity

To investigate the effect of treatment with continuous positive airway pressure (CPAP) on nocturnal polyuria in patients with obstructive sleep apnea syndrome (OSAS).. 15 patients with obstructive sleep apnea syndrome were included. The number of nocturia, the nocturia output, the osmotic pressure of nocturia and the nocturia excretion of Na(+) were recorded. Plasma levels of atrial natriuretic peptide (ANP) in night were measured in 8 patients. After treatment with CPAP, all the criteria were repeated.. (1) The number of nocturia decreased significantly after treatment with CPAP (P < 0.01); (2) The difference between nocturia output pre-and post treatment was significant (P < 0.01); (3) The osmotic pressure of nocturia rose from (381 +/- 96) mmol/L to (570 +/- 169) mmol/L (P < 0.05); (4) The nocturia excretion of Na(+) dropped from (1.16 +/- 0.35) mmol/h to (0.63 +/- 0.13) mmol/h (P < 0.01); (5) Plasma levels of ANP in night decreased from (146 +/- 14) ng/L to (106 +/- 10) ng/L (P < 0.01); (6) After treatment with CPAP, the reduction of ANP is correlated with the reduction of the nocturia output, the addition of the osmotic pressure of nocturia and the reduction of the nocturia excretion of Na(+). The correlation coefficients were 0.82, 0.84, 0.81 respectively.. Treatment with CPAP can reduce the number of nocturia, the nocturia output and the nocturia excretion of Na(+), increase the osmotic pressure of nocturia. The changes probably relate to the reduction of plasma level of ANP.

Topics: Adult; Atrial Natriuretic Factor; Circadian Rhythm; Humans; Male; Middle Aged; Polyuria; Positive-Pressure Respiration; Sleep Apnea, Obstructive

Topics: Atrial Natriuretic Factor; Endothelium, Vascular; Epoprostenol; Heart; Hemodynamics; Humans; Hypoxia; Nitric Oxide; Positive-Pressure Respiration; Renin-Angiotensin System; Sleep Apnea, Obstructive; Sleep, REM