Journal of hypertension · 2014
Relationship of circadian pattern of urine sodium excretion to hypertension and obstructive sleep apnoea.
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White Laura H, Bradley T Douglas, Logan Alexander G
Аннотация
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.
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.