This Article Full Text Full Text (PDF) All Versions of this Article: 49/5/e27    most recent HYPERTENSIONAHA.107.087908v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schlaich, M. P. Articles by Esler, M. D. Search for Related Content PubMed PubMed Citation Articles by Schlaich, M. P. Articles by Esler, M. D. Related Collections Other hypertension Clinical Studies Autonomic, reflex, and neurohumoral control of circulation

(Hypertension. 2007;49:e27.)
© 2007 American Heart Association, Inc.

Letters to the Editor

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

Baker Heart Research Institute, Melbourne, Australia

Paul A. Sobotka

ARDIAN Inc, Palo Alto, Calif

Gavin W. Lambert; Murray D. Esler

Baker Heart Research Institute, Melbourne, Australia

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Sympathetic activation is of crucial importance for both the blood pressure increase and the high morbidity and mortality in end-stage renal disease.¹ The mechanisms responsible for increased sympathetic outflow remain to be elucidated. In their latest of a series of informative studies in patients with chronic kidney disease (CKD), Neumann et al² report a reduction in muscle sympathetic nerve activity by decreasing the activity of the renin–angiotensin–system with angiotensin-converting enzyme inhibitors or angiotensin II type 1-receptor blockers, suggesting either a cause and effect relationship between the 2 or, alternatively, a common origin, such as kidney ischemia.

Although experimentally it is well established that angiotensin II facilitates norepinephrine release, its role in sympathetic activation in humans is less well documented. In another model of high sympathetic tone, namely, essential hypertension, we have used 2 different approaches to address these issues. First, in a randomized, placebo-controlled crossover study, we prospectively evaluated whether angiotensin II type 1-receptor blockers had identifiable antiadrenergic properties, as assessed by changes in muscle sympathetic nerve activity and whole body norepinephrine spillover.³ Despite comparable muscle sympathetic nerve activity (35±12 bursts per minute) in hypertensive patients on placebo compared with the CKD patients studied by Neumann et al (33±11 bursts per minute),² angiotensin II type 1-receptor blockers had no effect on either of the 2 parameters measured, indicating that the angiotensin II type 1-receptor blockers did not materially inhibit central sympathetic outflow or act presynaptically to reduce norepinephrine release at existing rates of nerve firing. In a . . . [Full Text of this Article]

This article has been cited by other articles:

				J. Neumann, G. Ligtenberg, I. H.T. Klein, P. Boer, P. L. Oey, H. A. Koomans, and P. J. Blankestijn Response to Sympathetic Hyperactivity in Hypertensive Chronic Kidney Disease Patients Is Reduced During Standard Treatment Hypertension, May 1, 2007; 49(5): e28 - e28. [Full Text] [PDF]