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Published Online
on January 15, 2007

Hypertension. 2007
Published online before print January 15, 2007, doi: 10.1161/01.HYP.0000256530.39695.a3
A more recent version of this article appeared on March 1, 2007
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Submitted on November 12, 2006
Revised on November 18, 2006

Sympathetic Hyperactivity in Hypertensive Chronic Kidney Disease Patients Is Reduced During Standard Treatment

Jutta Neumann; Gerry Ligtenberg; Inge H.T. Klein; Peter Boer; P. Liam Oey; Hein A. Koomans; and Peter J. Blankestijn*

From the Departments of Nephrology (J.N., G.L., I.H.T.K., P.B., H.A.K., P.J.B.) and Clinical Neurophysiology (P.L.O.), University Medical Center, Utrecht, the Netherlands.

* To whom correspondence should be addressed. E-mail: p.j.blankestijn{at}umcutrecht.nl.

Abstract--Standard treatment in chronic kidney disease (CKD) patients includes an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker. CKD is often characterized by sympathetic hyperactivity. This study investigates the prevalence of sympathetic hyperactivity (quantified by assessment of muscle sympathetic nerve activity [MSNA]) in a sizable group of patients with CKD and assessed whether chronic angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker normalizes increased MSNA. In 74 CKD patients (creatinine clearance 54±31 mL/min), MSNA, blood pressure, and plasma renin activity were measured in the absence of antihypertensive drugs except for diuretics. In a subgroup of 31 patients, another set of measurements was obtained after ≥6 weeks of enalapril (10 mg PO), losartan (100 mg PO), or eprosartan (600 mg PO). Patients as compared with control subjects (n=82) had higher mean arterial pressure (113±13 versus 89±7 mm Hg), MSNA (31±13 versus 19±7 bursts per minute), and log plasma renin activity (2.67±036 versus 2.40±0.32 fmol/L per second; all P<0.001). During angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker therapy (n=31), mean arterial pressure (115±11 to 100±9 mm Hg) and MSNA (33±11 to 25±9 bursts per minute) decreased (both P<0.01) but were still higher than in control subjects (both P<0.01). Multiple regression analysis identified age and plasma renin activity as predictive for MSNA. In conclusion, sympathetic hyperactivity occurs in a substantial proportion of hypertensive CKD patients. Angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker treatment reduces but does not normalize MSNA.


Key words: sympathetic hyperactivity • muscle sympathetic nerve activity • renal hypertension • chronic kidney disease • ACE inhibition • angiotensin II receptor blocker




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