Nocturnal Blood Pressure Decrease in Hypertensive Patients and Normotensives- Association with Obstructive Sleep Apnoea and Renal Function
Bodil G. Hornstrup1, 2, *, Jeppe B. Rosenbaek2, Nikolai Hoffmann-Petersen2, Pia H. Gjoerup2, Jost Wessels2, Thomas G. Lauridsen1, 2, Erling B. Pedersen1, Jesper N. Bech1, 2
1 University Clinic of Nephrology and Hypertension, Holstebro Hospital, Aarhus University, Holstebro, Denmark
2 Department of Medicine, Holstebro Hospital, Holstebro, Denmark
Blunted nocturnal Blood Pressure (BP) decrease is seen in patients with hypertension and obstructive sleep apnoea (OSA). The influence of OSA and renal function on nocturnal BP decrease is not fully clarified.
In this case control study of hypertensive patients and healthy controls, we aimed to analyse the relationship between nocturnal BP decrease on one hand and presence of OSA, renal function, plasma levels of syndecan and vasoactive hormones, and urinary sodium excretion on the other.
In 75 hypertensive patients and 56 controls, we performed brachial and central 24h ambulatory BP measurement and cardio respiratory monitoring. We measured syndecan, renin, angiotensinII, aldosterone, vasopressin, and brain natriuretic peptide in plasma and 24h urinary excretion of sodium, aquaporin2, and a component of the epithelial sodium channel (u-ENaCγ).
Nocturnal BP decrease was lower in patients than controls, brachial (13% versus 17%, p=0.001) and central (8% versus 10%, p=0.019). Moderate-to-severe OSA was present in 13% of patients, 2% of controls (p<0.005). Neither brachial nor central nocturnal BP decrease was associated with OSA, renal function, plasma levels of vasoactive hormones, syndecan-1, or urinary sodium excretion. P-syndecan and u-ENaCɣ were higher in patients than controls.
Both brachial and central nocturnal BP decrease was lower in patients than in controls. Neither brachial nor central nocturnal BP decrease was associated with the presence of OSA, renal function, or plasma levels of vasoactive hormones. Increased syndecan in plasma in hypertensive patients suggested damage to the endothelial glycocalyx.
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* Address correspondence to this author at the University Clinic of Nephrology and Hypertension, Holstebro Hospital, Aarhus University, Laegaardvej 12J, DK-7500 Holstebro, Denmark, Tel: 45 7843 6590; E-mail: firstname.lastname@example.org