Renal response to central volume expansion induced by water immersion (WI) in heart transplant patients

This work was aimed to assess the secretion of volume related hormones in heart transplant patients (HTP) and their relationship to excretory renal function studied under bed rest and water immersion conditions. Fractional sodium (FENa%) and potassium (FEK%) clearance, plasma renin activity (PRA), plasma aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) were estimated in six HTP with moderate renal failure (C creat = 69 +/- 6.9 ml/min) and in 10 healthy subjects (N) (C creat = 110 +/- 2.0 ml/min). All HTP were treated with cyclosporine A and azathioprine. In HTP basal AVP (6.18 +/- 0.92 pg/ml) and ANP (138.17 +/- 14.69 pg/ml) levels were significantly higher than in normals (2.07 +/- 0.11 pg/ml and 74.10 +/- 7.10 pg/ml, respectively). HTP were also characterized by increased FENa% and FEK% both under bed rest (DI) and water immersion (WI) conditions. As abnormalities of excretory renal function in HTP were not significantly related to the plasma endocrine profiles factors other than PRA, Ald, AVP and ANP seemed to be also involved in their pathogenesis.     

Influence of the redistribution of liquid volumes on atrial natriuretic factor

Several studies evidence that volume or pressure increase stimulates atrial natriuretic factor (ANF) secretion by atrial cardiocyte stretch. In order to study the relationship between plasma renin activity (PRA) and ANF plasma level in experimental weightlessness, six healthy male subjects were submitted to antigravity (anti-g) suit inflation which shifts fluid in the thoracic region. Firstly, blood samples were taken at rest after 15 mn in supine position, secondly after 25 mn in upright position with and without anti-g suit. During the tilt test, plasma ANF decreased from 35 +/- 4.1 to 28 +/- 6.6 pg/ml (p less than 0.05) without anti-g suit and rose to 38 +/- 4.1 pg/ml (p less than 0.05) with anti-g suit. This demonstrates the stimulating effect of weightlessness on the ANF release. During the same tilt test PRA increased from 2.69 +/- 0.29 to 4.76 +/- 0.83 ng/ml/h that evidences the perfusion pressure fall on the intrarenal baroreceptors. Anti-g suit inflation abolished this PRA response to the orthostatism, since PRA increase was only 3.23 +/- 0.79 ng/ml/h (p less than 0.05). ACTH and aldosterone levels do not change significantly. These results demonstrate that ANF and PRA which have opposite effects on aldosterone release and Na excretion, change in opposite sens during fluid shifts, to produce antinatriuresis in upright position, or natriuresis in experimental weightlessness.     

The plasma atrial natriuretic peptide response to arm and leg exercise in humans: effect of posture

During arm exercise (A), mean arterial pressure (MAP) is higher than during leg exercise (L). We evaluated the effect of central blood volume on the MAP response to exercise by determining plasma atrial natriuretic peptide (ANP) during moderate upright and supine A, L and combined arm and leg exercise (A + L) in 11 male subjects. In the upright position, MAP was higher during A than at rest (102 +/- 6 versus 89 +/- 6 mmHg; mean +/- s.d.) and during L (95 +/- 7 mmHg; P < 0.05), but similar to that during A + L (100 +/- 6 mmHg). There was no significant change in plasma ANP during A, while plasma ANP was higher during L and A + L (42.7 +/- 12.2 and 43.3 +/- 17.1 pg ml(-1), respectively) than at rest (34.6 +/- 14.3 pg ml(-1), P < 0.001). In the supine position, MAP was also higher during A than at rest (100 +/- 7 versus 86 +/- 5 mmHg) and during L (92 +/- 5 mmHg; P < 0.01) but similar to that during A + L (102 +/- 6 mmHg). During supine A, plasma ANP was higher than at rest and during L but lower than during A + L (73.1 +/- 22.5 versus 47.2 +/- 15.9, 67.4 +/- 18.3 and 78.1 +/- 25.0 pg ml(-1), respectively; P < 0.05). Thus, upright A was the exercise mode that did not enhance plasma ANP, suggesting that central blood volume did not increase. The results suggest that the similar blood pressure response to A and to A + L may relate to the enhanced central blood volume following the addition of leg to arm exercise.     

Alterations of vasoconstrictor and sodium-regulating hormone systems in vascularly decompensated liver cirrhosis

Plasma levels of atrial natriuretic peptide (ANP), aldosterone (PA), vasopressin (AVP), and the plasma renin activity (PRA) were examined in 15 vascularly decompensated patients suffering from liver cirrhosis, before and after administration of albumin and after a subsequent administration of furosemide. The initial ANP level was lower in 9 patients (group "A") and higher in 6 patients (group "B") than in healthy controls (Group "A": 19.5 +/- 3.0 fmol/ml; group "B": 36.7 +/- 3.9 fmol/ml; control: 25.8 +/- 2.4 fmol/ml). The initial PRA (4.4 +/- 1.0 ng AngI/ml/h) and AVP (8.5 +/- 1.5 pg/ml) activity in group "A" increased significantly compared to group "B" (PRA: 0.44 +/- 0.09; AVP: 4.1 +/- 0.5), indicating an intravascular volume depletion in group "A". Albumin infusion raised the urine and sodium excretion and the plasma concentration of ANP in group "A" but lowered in plasma levels of renin and vasopressin. The same parameters were not changed by albumin in group "B". Furosemide equally raised the urine flow rate and sodium excretion in both groups. Plasma ANP level depends on the intravascular volume, and the secondary change in its plasma concentration plays a considerable role in the retention of fluid and electrolytes in patients with cirrhosis. The increased intravascular volume in these patients depletes the fluid and electrolyte retention via the increase in ANP level.     

Basal and stimulated plasma atrial natriuretic peptide (ANP) concentrations and cardiac ANP contents in old and young rats.

To investigate the ability of the ageing heart to release atrial natriuretic peptide (ANP) we compared the response of awake, trained, chronically catheterized old (20-21 months) and young (4 months) rats to an acute, hypertonic saline challenge. There were no differences between young and old rats in basal plasma concentration of sodium (PNa; old: 141 +/- 3 meq/l; young: 143 +/- 3 meq/l) or ANP (old: 61 +/- 5 pg/ml; young: 67 +/- 12 pg/ml). Five minutes after acute saline challenge, PNa rose in both groups (old: 146 +/- 2 meq/l; young 149 +/- 1 meq/l) and approximately 3-fold increases in plasma ANP levels (182 +/- 24 pg/ml; young: 179 +/- 42 pg/ml). Hearts of old and young rats were assayed for atrial and ventricular ANP content. Atrial ANP levels were similar in old and young rats (13.5 +/- 3.6 vs. 24.9 +/- 8.7 micrograms/g atrial tissue), whereas ventricular ANP content was approximately 4-fold higher in old vs. young rats (153.7 +/- 39.3 vs. 47.5 +/- 6.4 ng/g ventricular tissue). Thus, the ageing rat heart responds equally as well as the young rat to an acute NaCl challenge.     

Heterologous radioimmunoassay of atrial natriuretic polypeptide in dog and rabbit plasma

Atrial natriuretic peptide (ANP) was measured in plasma of dogs and rabbits by radioimmunoassay (RIA) using a commercially available anti alpha-ANP serum and compared to our measurements of ANP in rats and humans. Plasma concentration of ANP in dog coronary sinus (234.9 +/- 41.0 pg/ml) was significantly greater than in systemic arterial blood (81.2 +/- 8.4 pg/ml). Gel filtration of dog coronary sinus plasma resulted in an ANP peak with the elution volume (Ve) of synthetic atriopeptin III (AIII) and a minor peak eluting with the void volume (Vo). Rabbit systemic arterial plasma ANP was 53.3 +/- 4.3 pg/ml and yielded one peak, with a Ve of AIII. Ion exchange chromatography of dog and rabbit atrial extracts (AE) resulted in a major ANP region which resembled AIII. Gel filtration of AE showed larger molecular species as well as AIII. Dilutions of dog and rabbit plasma and AE were parallel with the AIII standard in radioimmunoassay.     

Influence of endogenous opioids on atrial natriuretic factor release during exercise in man

Summary To evaluate to what extent opioid secretion in exercise induces the release of atrial natriuretic factor (ANF), six healthy male volunteers who were trained subjects, were submitted to two maximal exercise tests with and without (control) opioid receptor blockade by Naltrexone. Blood samples were drawn before (rest) and after exercise (post-exercise) in order to measure human ANF (αh ANF),β-endorphin, plasma aldosterone concentration (PAC) plasma renin activity (PRA) and adreno-cortico trophic hormone (ATCH) by radio-immunological methods. Expired gas was collected during exercise to measure oxygen consumption. On average, the same maximal oxygen consumption ( ) during exercise was reached by all subjects with and without treatment. Plasma ANF level at rest slightly decreased after administration of Naltrexone; the response to physical exercise was significantly reduced by Naltrexone. There was no statistical difference between plasma levels ofβ-endorphin, PRA and ACTH at rest nor in the post-exercise situation under the influence of Naltrexone. The PAC increased significantly at rest after Naltrexone administration but there was no statistical difference between both values after exercise. These data demonstrate that: (1) ANF secretion during exercise is influenced by the level ofβ-endorphin in the plasma; (2) the possible inhibitory role of ANF on aldosterone secretion during exercise is probably over-ruled by the increase in plasma ACTH and PRA.     

Plasma atrial natriuretic peptide in DOCA-NaCl-treated rats

In order to assess the possible role of atrial natriuretic peptide (ANP) in the development of deoxycorticosterone (DOCA)-NaCl-induced hypertension, plasma immunoreactive ANP concentration was compared with sodium balance and blood pressure in NaCl- or DOCA-NaCl-treated rats. Both NaCl-and DOCA-NaCl-loading increased plasma ANP levels (to 86 +/- 8.1 and 105 +/- 12 pg ml-1 respectively; 47 +/- 6.7-60 +/- 4.6 pg ml-1 in controls), which were correlated to sodium intake and excretion. In DOCA-NaCl-treated rats, the highest ANP levels (105 +/- 12 pg ml-1) were found 4 weeks after the beginning of DOCA-NaCl treatments. Along with the development of DOCA-NaCl hypertension in 1-kidney-DOCA-NaCl-treated rats, however, plasma ANP concentration did not rise further. We conclude that secretion of ANP into the circulation is increased during DOCA-NaCl treatment. Elevated blood pressure does not stimulate ANP release in DOCA-NaCl-treated rats further.     

Effect of beta 1-adrenoceptor blockade on plasma levels of atrial natriuretic peptide during exercise in normal man

Increased plasma levels of atrial natriuretic peptide (ANP) during exercise have been reported. To investigate the role of tachycardia as a stimulus for release of ANP during exercise the following study was undertaken. Graded exercise was performed in six healthy volunteers before and after beta 1-adrenoceptor blockade. Plasma levels of ANP were determined at different workloads in both cases. At rest and at all workloads during exercise plasma levels of ANP were higher after beta 1-adrenoceptor blockade than without. Therefore, it is unlikely that tachycardia is a major stimulus for secretion of ANP during exercise. It is suggested that increased right atrial pressure and/or pulmonary arterial blood pressure and increased plasma levels of catecholamines are important secretory stimuli for ANP during exercise.     

The existence of low concentrations of atrial natriuretic peptide (ANP) in canine cerebrospinal fluid which does not correlate with plasma ANP levels

Atrial natriuretic peptide (ANP) concentrations in the cerebrospinal fluid (CSF) and plasma of canine were 2.1 +/- 1.1 pg/ml (mean +/- S.D.) and 53.1 +/- 21.1 (n = 20), respectively. The regression coefficient between these concentrations was -0.0045 (P = n.s.). The ANP concentration in the CSF did not change even after the plasma ANP concentration was altered following the change of left atrial pressure, as in 4 cases of an experimental aortic regurgitation. Thus, ANP concentration in the CSF is not influenced by ANP concentrations in the plasma at least under our condition. Gel permeation chromatography revealed a single form of ANP in the position of authentic alpha-ANP in canine CSF, while a high molecular weight ANP peak was observed as well as alpha-ANP in the plasma.     

Concomitant increase in plasma atrial natriuretic peptide and cyclic GMP during volume loading

Summary To investigate the effects of fluid expansion on endogenous atrial natriuretic peptide (ANP) and cyclic 3,5-guanosine monophosphate (cGMP), four male volunteers were studied before, during and after intravasal volume loading. Volume expansion was performed by intravenous infusion of 2,000 ml isotonic saline solution within 30 min. Mean plasma ANP levels increased 2.5-fold from 31.2 pg/ml to 81.7 pg/ml 40 min after the start of infusion. Plasma cGMP levels paralleled the rise in ANP, shwoing a mean cGMP increment from 2.7 pmol/ml to a maximum of 8.2 pmol/ml. Both ANP and cGMP levels were back to basal levels 120 min after termination of the infusion. Stimulation of endogenous ANP release by volume loading suggests that ANP is involved in the regulation of fluid homeostasis in man. The parallel rise in plasma cGMP levels supports the idea that cGMP is a mediator for the effects of ANP.Abbreviations ANP atrial natriuretic peptid - cGMP cyclic 3,5-guanosine monophosphate - PRA plasma renin activity     

Effects of physical exercise and anti-G suit inflation on atrial natriuretic factor plasma level

Summary The purpose of this study was to measure the effect of enhanced venous return on atrial natriuretic factor (ANF) secretion during exercise and upright posture and the consequences on renin angiotensin aldosterone system (RAAS) activity. Six healthy male subjects were submitted to four different procedures. All procedures were performed in the same position, i.e. riding on a support with legs hanging. Two procedures were performed at rest: the subjects were studied after a 25-min rest in this position, with and without the lower limb fitted with an anti-G suit inflated to 60 mmHg. Two procedures were carried out with physical exercise; arm-cranking was performed in the same position with and without the anti-G suit inflated to 60 mmHg. Venous blood was collected before and after each procedure in order to measure plasma ANF, plasma aldosterone concentration (PAC), plasma renin activity (PRA), corticotrophin (ACTH) and catecholamine level. The data mean ±SEM showed that the ANF plasma level decreased significantly (p<0.05) from 32.5±4 to 28±6 pg · ml⁻¹ after a 20-min rest in the upright posture, whereas this effect was absolished with anti-G suit inflation. Physical exercise with and without the anti-G suit increased the ANF level above control values (60±13.6 pg · ml⁻¹ and 53±13 pg · ml⁻¹): anti-G suit inflation had no significant effect. PRA increased after rest in an upright posture and during physical exercise; anti-G suit inflation abolished this increase in both conditions. PAC was not influenced by postural change but significantly increased in all exercise tests. ACTH increased to the same extent in both exercise tests. The plasma catecholamine level increased during upright posture and both physical exercise procedures. These results indiate that enhanced venous return during anti-G suit inflation increases ANF secretion at rest in an upright posture and that physical exercise greatly increases plasma ANF level independently of the anti-G suit inflation. They suggest that ANF release during exercise could be influenced by factors other than haemodynamic stimuli. The comparison between ANF and PRA changes during arm-cranking indicates that PRA is influenced more than ANF by blood volume displacement. The ANF increase during exercise does not inhibit aldosterone secretion.     

Plasma atrial natriuretic factor in low output heart failure syndromes

Summary Plasma atrial natriuretic factor, aldosterone, renin activity, and antidiuretic hormone were studied in low output heart failure syndromes: cardiogenic shock in ten patients with acute myocardial infarction of the anterior wall (first group), hypovolemic shock after melena from peptic ulcer in ten subjects (second group), and hypotension with bradycardia syndrome in ten patients with acute myocardial infarction of the inferior wall (third group). Circulating atrial natriuretic factor in patients with cardiogenic shock (102.4±7.4 pg/ml) was significantly higher than in healthy volunteers matched for sex and age (8.4±0.3 pg/ml). In these patients there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the second and third groups were within normal range. Plasma aldosterone was high in all groups, plasma renin activity was elevated in the first and third groups, and high antidiuretic hormone was observed in the first and second groups. These findings indicate that in low output heart failure syndromes only hemodynamic changes affecting the atria stimulate atrial natriuretic factor release. No correlations were found between plasma atrial natriuretic factor and other hormones. In particular, high atrial natriuretic factor levels in the patients with cardiogenic shock did not inhibit release of aldosterone, renin, or antidiuretic hormone. It may be surmised that in these patients the hemodynamic effects override the inhibitory effects of atrial natriuretic factor.Abbreviations ANF atrial natriuretic factor - ANP atrial natriuretic peptide - ANOVA analysis of variance - ACTH adrenocorticotropin hormone     

Atrial natriuretic peptide secretion in heart transplant patients

Plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA), aldosterone (ALD) and vasopressin (VP) were assessed in six heart transplant patients (HTP) and ten healthy subjects under bed rest conditions and 60 and 120 minutes after head-out water immersion (WI). Bed rest had no significant influence on these parameters. WI raised plasma volume (PV) to the same extent in both groups. This increase of PV was accompanied by significant suppression of PRA, ALD and VP and an increase of plasma ANP. In HTP basal plasma ANP was significantly elevated and the ANP response to central hypervolemia reduced. Significantly elevated VP plasma levels were also found in HTP. These endocrine abnormalities in HTP seem to be caused by latent failure of the transplanted heart. No direct correlation was found between plasma ANP and PRA, ALD and VP under basal conditions and after WI in either HTP or normals.     

Atrial natriuretic peptide and catecholamines in obstructive sleep apnea syndrome.

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.     

The use of a monoclonal antibody for the determination of atrial natriuretic peptides in human plasma

Summary A monoclonal antibody (mab) directed against -human atrial natriuretic peptides (-hANP) was produced. Using this mab a radioimmunoassay for the determination of hANP-like immunoreactivity in human plasma was established. To demonstrate the possible application of this radioimmunoassay for clinical diagnosis, plasma levels were measured in healthy subjects and in patients with renal failure before and after hemofiltration or hemodialysis. Plasma levels in healthy subjects ranged between less than 30 and 124 pg/ml. Mean plasma concentrations of hANP-IR in uremic subjects were 324 pg/ml before and 113 pg/ml after hemofiltration or hemodialysis.Abbreviations ANP atrial natriuretic peptides - hANP human atrial natriuretic peptide - hANP-IR hANP-like immuno-reactivity - HPLC high performance liquid chromatography - mab monoclonal antibody - RIA radioimmunoassay     

Atrial-specific granule number and plasma atrial natriuretic peptide in rats: effects of beta-adrenoceptor blockade and sodium intake

An interrelationship between atrial natriuretic peptide (ANP) and the renin-angiotensin system has been established. Both of these hormonal systems are modulated by sodium balance. The role of the beta-adrenoceptor in the regulation of release of ANP is not clear. We therefore undertook a study to examine changes in atrial-specific granule number and plasma ANP level following beta-adrenoceptor blockade in rats on low and high sodium intakes. A low-sodium diet, as compared with a high-sodium diet, elevated right and left atrial-specific granule number (right atria 54.6 +/- 8.7 vs. 42.3 +/- 5.7; left atria 47.7 +/- 7.7 vs. 30.6 +/- 3.4 granules/unit area) and plasma renin activity (28 +/- 3.7 vs. 5.4 +/- 0.8 ng AI/ml/hr). Plasma ANP levels were lower in the low-sodium animals (98 +/- 34 vs. 345 +/- 38 pg/ml). When treated with the nonspecific beta-adrenoceptor blocker propranolol, the elevated plasma renin activity and atrial-specific granule number in rats on a low sodium intake were significantly less. Neither of these parameters changed in rats on a high sodium intake. Conversely, propranolol treatment resulted in lower plasma ANP levels in rats with high sodium intake. The already-suppressed plasma ANP level in rats on a low-sodium diet was unaltered with beta-adrenoceptor blockade. The results suggest that dietary sodium intake is an important determinant of the response of atrial-specific granule number and plasma ANP levels following beta-adrenoceptor blockade with propranolol.     

Increased brain natriuretic peptide and atrial natriuretic peptide plasma concentrations in dialysis-dependent chronic renal failure and in patients with elevated left ventricular filling pressure

Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations were measured in patients with dialysis-dependent chronic renal failure and in patients with coronary artery disease exhibiting normal or elevated left ventricular end-diastolic pressure (LVEDP) (n = 30 each). Blood samples were obtained from the arterial line of the arteriovenous shunt before, 2 h after the beginning of, and at the end of hemodialysis in patients with chronic renal failure. In patients with coronary artery disease arterial blood samples were collected during cardiac catheterization. BNP and ANP concentrations were determined by radioimmunoassay after Sep Pak C₁₈ extraction. BNP and ANP concentrations decreased significantly (P < 0.001) during hemodialysis (BNP: 192.1 ± 24.9, 178.6 ± 23.0, 167.2 ± 21.8 pg/ml; ANP: 240.2 ± 28.7, 166.7 ± 21.3, 133.0 ± 15.5 pg/ml). The decrease in BNP plasma concentrations, however, was less marked than that in ANP plasma levels (BNP 13.5 ± 1.8%, ANP 40.2 ± 3.5%; P < 0.001). Plasma BNP and ANP concentrations were 10.7 ± 1.0 and 60.3 ± 4. 0 pg/ml in patients with normal LVEDP and 31.7 ± 3.6 and 118.3 ± 9.4 pg/ml in patients with elevated LVEDP. These data demonstrate that BNP and ANP levels are strongly elevated in patients with dialysis-dependent chronic renal failure compared to patients with normal LVEDP (BNP 15.6-fold, ANP 2.2-fold, after hemodialysis; P < 0.001 or elevated LVEDP (BNP 6.1-fold, ANP 2.0-fold, before hemodialysis; P < 0.001), and that the elevation in BNP concentrations was more pronounced than that in ANP plasma concentrations. The present results provide support that other factors than volume overload, for example, decreased renal clearance, are also involved in the elevationin BNP and ANP plasma levels in chronic renal failure. The stronger elevation in BNP concentrations in patients with chronic renal failure and in patients with elevated LVEDP and the less pronounced decrease during hemodialysis suggest a different regulation of BNP and ANP plasma concentrations.[/ p]Abbreviations ANP atrial natriuretic peptide - BNP brain natriuretic peptide - LVEDP left ventricular end-diastolic pressure Correspondence to: C. Haug     

Atrial natriuretic excretion in patients with obstructive sleep apnea syndrome (OSAS)

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. CONCLUSIONS: 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.