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To assess the acute effects of nasal continuous positive airway pressure (CPAP) on the 24-hour blood pressure and the secretion of catecholamines in urine and plasma, we investigated the changes in the 24-hour blood pressure and urinary and plasma concentrations of epinephrine (E) and norepinephrine (NE) in 26 men with obstructive sleep apnea (OSA) with and without nasal CPAP. Nasal CPAP resulted in significant decreases in the daytime diastolic pressure (from 86 +/-16 mmHg to 83+/-12 mmHg), the nighttime diastolic pressure (from 81+/-12 mmHg to 77+/-9 mmHg) and the nighttime systolic pressures (from 125+/-15 mmHg to 120+/-10 mmHg). There was no significant difference between patients with and without CPAP in the daytime or nighttime urinary E level, but patients who received CPAP showed a significant decrease in daytime urinary NE level (from 156+/-112 microg/14h to 119+/-101 microg/14h) and nighttime urinary NE level (from 143+/-91 microg/10h to 112+/-65 microg/10h). The morning plasma level of NE also decreased (from 371+/-181 pg/ml to 273 +/-148 pg/ml) in patients who received nasal CPAP (p<0.02), but the plasma level of E remained unchanged. There were no correlations between PSG parameters and the reductions in blood pressure and the catecholamine levels induced by nasal CPAP. These findings suggest that OSA contributes, at least in part, to the development of systemic hypertension by increasing sympathetic nervous activity.

Study Objective: To assess the utility of urinary uric acid excretion as a marker of nocturnal hypoxia in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) before and after the institution of nasal continuous positive airway pressure (CPAP)., Design: Prospective, open., Setting: Sleep Disorders Laboratory, Veterans Affairs Medical Center., Participants: Thirty consecutive male subjects, 20 with OSAHS and 10 without OSAHS., Measurements and Methods: Spot morning urine and venous blood samples were obtained in all subjects; samples were also obtained after the application of CPAP in those with OSAHS. Uric acid excretion, normalized to creatinine clearance, was calculated as the product of urinary uric acid and serum creatinine concentrations divided by urine creatinine concentration. In patients with OSAHS, uric acid excretion was 0.55+/-0.1 mg/dL before CPAP therapy and decreased to 0.30+/-0.01 mg/dL after CPAP therapy (p < 0.001). The latter value did not differ significantly from the mean value (0.32+/-0.03 mg/dL) in the control group. Uric acid excretion in OSAHS patients correlated significantly with the apnea-hypopnea index (r=0.42; p<0.0003)., Conclusion: Uric acid excretion is increased in OSAHS patients and normalizes after CPAP treatment, most likely reflecting differences in tissue oxygenation between the two conditions. Further studies in large number of patients may confirm the usefulness of this simple test for diagnosis and follow-up of patients with OSAHS.

During hypoxia ATP degradation to uric acid is increased in animal models and humans. To assess the reliability of an overnight increase in uric acid excretion as a marker of nocturnal hypoxemia, we selected 10 normal volunteers (7 males and 3 females), 29 COPD patients (26 males and 3 females), and 49 subjects with obstructive sleep apnea (OSA) (43 males and 6 females). The patients underwent standard polysomnography, which was repeated in 14 subjects with nasal continuous positive airway pressure (CPAP), and were subdivided into two groups: Group D included desaturating subjects who spent at least 1 h at SaO2 < 90% and 15 min below 85%, and Group ND were nondesaturating subjects. The overnight change in the uric acid:creatinine ratio (delta UA:Cr) was negative in normal subjects (-27.5 +/- 9.1 [mean +/- SD]) and ND groups: -19.7 +/- 14.3 in COPD, -16.1 +/- 13.0 in OSA. In both COPD and OSA Group D, the ratio was usually positive: delta UA:Cr was 17.9 +/- 31.4 in Group D COPD (p < 0.001 versus ND) and 10.1 +/- 30.7 in Group D OSA (p < 0.001 versus ND and versus normal subjects) despite 4 of 15 false negative results in COPD and 8 of 20 in OSA. CPAP effective treatment induced a marked reduction ((p = 0.0024) in delta UA:Cr, leading to a negative value. We conclude that delta UA:Cr seems to be a promising index of significant nocturnal tissue hypoxia, with good specificity but poor sensitivity (about 30% false negative), which might be useful for the long-term follow-up of outpatients on nasal CPAP with a positive ratio at baseline.

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.

To clarify the paradox of a decrease in urine and sodium excretion occurring along with the elimination of peripheral edema when patients with obstructive sleep apnea (OSA) are treated with nasal continuous positive airway pressure (CPAP), we investigated the immediate effects of this treatment on the hematocrit and red blood cell count in eight patients with OSA. The hematocrit decreased in all patients, from a mean of 45.6 +/- 1.2 percent to 43.0 +/- 1.4 percent, with a parallel decrease in the red blood cell count from 4.777 +/- 0.168 millions/cu mm to 4.577 +/- 0.174 millions/cu mm (p less than 0.0005, one-tailed, in both cases). These results suggest that nasal CPAP treatment causes a hemodilution in patients with OSA, and are compatible with the hypothesis of an atrial natriuretic peptide-induced fluid shift from the intravascular to the extravascular volume in untreated patients with OSA. The reversal of these changes with CPAP treatment could explain the simultaneous decrease in sodium and urine excretion and the reduction of peripheral edema.

Obstructive sleep apnea (OSA) patients have increased diuresis and natriuresis during sleep. In order to investigate the possible mechanisms of these changes in renal function, 35 consecutively diagnosed OSA patients were studied during sleep before and during nasal continuous positive airway pressure (CPAP) treatment, and were compared with 23 non-snoring controls. The excretion of urine and of electrolytes was increased before treatment and normalized with nasal CPAP treatment. The mechanism involved seems to be decreased sodium reabsorption at the level of the ascending limb of the loop of Henle. The observed increase in cyclic guanosine monophosphate excretion supports the hypothesis of increased atrial natriuretic peptide release during sleep in OSA patients.

Patients with obstructive sleep apnea (OSA) often exhibit nocturnal polyuria, which disappears with nasal continuous positive airway pressure (CPAP) treatment. We measured water and electrolyte urinary excretion, creatinine and osmolal clearances, and water transport during sleep in 13 polygraphically monitored patients with OSA during two consecutive nights, either untreated or treated with nasal CPAP, and in eight normal subjects. Untreated patients with OSA had greater urinary flows and greater urinary sodium, chloride, and potassium excretions than did controls. Nasal CPAP treatment in patients with OSA resulted in a reduction in urinary flow and in sodium and chloride excretion, with a concomitant increase in sodium resorption. None of these effects was observed in CPAP-treated normal subjects. The only effect of nasal CPAP common to normal subjects and patients was a trend toward decreased glomerular filtration rate.