Laura H White1, T Douglas Bradley, Alexander G Logan. 1. aSleep Research Laboratory, Toronto Rehabilitation Institute bCentre for Sleep Medicine and Circadian Biology of the University of Toronto cDepartment of Medicine of the University Health Network, Toronto General Hospital and Mount Sinai Hospital dLunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital eFaculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Abstract
OBJECTIVES: Obstructive sleep apnoea (OSA) and hypertension frequently coexist, and both are associated with higher night-time than daytime urine sodium excretion rate (UNaV). However, the relative contribution of each condition is unknown. We compared the circadian pattern of UNaV in hypertensive and normotensive patients with and without OSA. METHODS: Hypertensive [blood pressure (BP) >140/90 or on antihypertensive medications, excluding diuretics] and normotensive (BP <135/85) patients underwent overnight polysomnography to determine the presence or absence of OSA (apnoea-hypopnoea index ≥10 or <10, respectively), same-day 24-h urine collection divided into day and night-time samples and automated evening BP measurement. RESULTS: Twenty-six hypertensive (9 without and 17 with OSA) and 26 normotensive (15 without and 11 with OSA) patients were studied. Night-time UNaV was higher in the hypertensive than the normotensive patients. Whereas in the normotensive patients night-time UNaV was unaffected by OSA, in the hypertensive patients, it was higher in those with than without OSA (P = 0.009 for OSA × hypertension interaction). Night : day UNaV ratio was higher in hypertensive than normotensive patients, but was not significantly affected by OSA in either group. On multivariate analysis, SBP and apnoea-hypopnoea index were independent predictors of night-time UNaV (model r = 0.574, P < 0.001) and night : day UNaV ratio (model r = 0.397, P < 0.001). However, SBP was the strongest independent predictor. CONCLUSIONS: In hypertensive patients, OSA exacerbates the reversal of the normal circadian sodium excretion pattern by elevating nocturnal UNaV, possibly via its BP-elevating effects. However, OSA does not affect nocturnal UNaV in normotensive patients.
OBJECTIVES:Obstructive sleep apnoea (OSA) and hypertension frequently coexist, and both are associated with higher night-time than daytime urine sodium excretion rate (UNaV). However, the relative contribution of each condition is unknown. We compared the circadian pattern of UNaV in hypertensive and normotensive patients with and without OSA. METHODS:Hypertensive [blood pressure (BP) >140/90 or on antihypertensive medications, excluding diuretics] and normotensive (BP <135/85) patients underwent overnight polysomnography to determine the presence or absence of OSA (apnoea-hypopnoea index ≥10 or <10, respectively), same-day 24-h urine collection divided into day and night-time samples and automated evening BP measurement. RESULTS: Twenty-six hypertensive (9 without and 17 with OSA) and 26 normotensive (15 without and 11 with OSA) patients were studied. Night-time UNaV was higher in the hypertensive than the normotensive patients. Whereas in the normotensive patients night-time UNaV was unaffected by OSA, in the hypertensivepatients, it was higher in those with than without OSA (P = 0.009 for OSA × hypertension interaction). Night : day UNaV ratio was higher in hypertensive than normotensive patients, but was not significantly affected by OSA in either group. On multivariate analysis, SBP and apnoea-hypopnoea index were independent predictors of night-time UNaV (model r = 0.574, P < 0.001) and night : day UNaV ratio (model r = 0.397, P < 0.001). However, SBP was the strongest independent predictor. CONCLUSIONS: In hypertensivepatients, OSA exacerbates the reversal of the normal circadian sodium excretion pattern by elevating nocturnal UNaV, possibly via its BP-elevating effects. However, OSA does not affect nocturnal UNaV in normotensive patients.