Abstract
Objective. 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. Material and methods. 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 (FENa), free water clearance (CH2O), urinary excretion of aquaporin 2 (u‐AQP2), systolic blood pressure (SBP), diastolic blood pressure (DBP) and oxygen saturation. Results. OSA patients had a higher FENa (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 FENa correlated significantly with the change in nocturnal DBP (r2 = 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, CH2O and u‐AQP2 were the same in OSA and controls. Conclusions. 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.
Acknowledgements
The study was supported by Ringkjobing County, the Research Foundation of Ringkjobing County and the Danish Lung Association. We thank laboratory technicians at the Department of Medical Research, Holstebro Hospital for skilful technical assistance and commitment and the staff at the Section of Pulmonary Diseases, Department of Medicine, Holstebro Hospital for their kind assistance in the realization of this study.