Abstract
Objectives: We have studied circadian blood pressure (BP) rhythm in patients with CKD using the night/day ratio of BP obtained by 24-h ABPM, and postulated that impaired renal sodium excretion causes insidious sodium-fluid retention to promote night-time hypertension. Emerging evidences suggest that, in addition to sodium-fluid retention and hyperactivity of the renin-angiotensin-aldosterone system, increased autonomic nervous system activity contributes to the genesis of hypertension in CKD. Methods: study 1. Relationship between the heart rate variability (HRV) obtained by Holter ECG (e.g., LF/HF, HF) and variables obtained by ABPM [e.g., day/night HR ratio, coefficient of variation (CV) of HR] were investigated.study 2. We examined the relationship between day/night ratios of HR and HF, as well as CV, before and during 8 week treatment with angiotensin II receptor blocker (ARB), which are known to suppress the sympathetic nerve activity (olmesartan 2.5-40 mg/day) in 45 CKD patients. Results: study 1. 24-h HF, ln(ms2) directly correlated with day/night HR ratio and CV of HR. study 2. ARB increased the day/night HR ratio (1.17 to 1.21, p = 0.04), and CV of HR (16 to 17%, NS). Day/night ratio of (HR/MAP) correlated inversely with the GFR (p = 0.04). This correlation did not persist during the treatment with ARB. Conclusions: The present study demonstrated that the increase in the CV and day/night ratio of HR provided by ABPM indicate the elevated parasympathetic activity shown by Holter ECG, and that autonomic nervous system activityis activated as renal function deteriorates, and ARB may suppress its activation.
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