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(Hypertension. 2007;49:e28.)
© 2007 American Heart Association, Inc.

Letters to the Editor

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

Jutta Neumann; Gerry Ligtenberg; Inge H.T. Klein; Peter Boer

Department of Nephrology, University Medical Center, Utrecht, The Netherlands

P. Liam Oey

Department of Clinical Neurophysiology, University Medical Center, Utrecht, The Netherlands

Hein A. Koomans; Peter J. Blankestijn

Department of Nephrology, University Medical Center, Utrecht, The Netherlands

An extract of the first 100% of the full text is provided, because this article has no abstract.

We thank Schlaich et al¹ for their comment. We fully agree that the pathogenesis may vary in the various disease conditions known to have sympathetic hyperactivity. Essential hypertension is a heterogenous condition. Indeed, apart from their studies, several other investigators have shown that angiotensin-converting enzyme inhibitor and/or angiotensin II antagonists have little or no effect on sympathetic activity in essential hypertensive patients.^2–4 On the other hand, the landmark article by Converse et al,⁵ in which they show that dialysis patients with their native kidneys still present have high muscle sympathetic nerve activity, whereas bilaterally nephrectomized dialysis patients have muscle sympathetic nerve activity comparable to control subjects, provides definite proof that the diseased kidneys are critically involved in the pathogenesis of sympathetic hyperactivity. Experimental evidence has shown that already limited kidney damage, not necessarily affecting kidney function, can result in sympathetic activation.⁶ We put forward that, apart from chronic kidney disease, such a condition of (limited) kidney damage may be present in many disease states, resulting in activation of both the renin and the sympathetic system.

Disclosures

None.

1. Schlaich MP, Lamber EA, Sobotka PA, Lambert GW, Esler MD. Sympathetic hyperactivity in hypertensive chronic kidney disease patients is reduced during standard treatment. Hypertension. 2007; 49: e27.[Free Full Text]

2. Grassi G, Turri C, Dell’Oro R, Stella ML, Bolla GB, Mancia G. Effect of chronic angiotensin converting enzyme inhibition on sympathetic nerve traffic and baroreflex control of the circulation in essential hypertension. J Hypertens. 1998; 16: 1789–1796.[CrossRef][Medline] [Order article via Infotrieve]

3. Struck J, Muck P, Trubger D, Handrock R, Weidinger G, Dendorfer A, Dodt C. Effects of selective angiotensin II receptor blockade on sympathetic nerve activity in primary hypertensive subjects. J Hypertens. 2002; 20: 1143–1149.[CrossRef][Medline] [Order article via Infotrieve]

4. Bechir M, Enseleit F, Chenevard R, Luscher TF, Noll G. Effect of losartan on muscle sympathetic activity and baroreceptor function in systemic hypertension. Am J Cardiol. 2005; 95: 129–131.[CrossRef][Medline] [Order article via Infotrieve]

5. Converse RL Jr, Jacobsen TN, Toto RD, Jost CM, Cosentino F, Fouad-Tarazi F, Victor RG. Sympathetic overactivity in patients with chronic renal failure. N Engl J Med. 1992; 327: 1912–1918.[Abstract]

6. Ye S, Gamburd M, Mozayeni P, Koss M, Campese VM. A limited renal injury may cause a permanent form of neurogenic hypertension. Am J Hypertens. 1998; 11: 723–728.[CrossRef][Medline] [Order article via Infotrieve]