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J Am Soc Nephrol 11:1469-1478, 2000
© 2000 American Society of Nephrology

Effects of Low Dose Sympathetic Inhibition on Glomerulosclerosis and Albuminuria in Subtotally Nephrectomized Rats

KERSTIN AMANN*,{dagger}, LARS CHRISTIAN RUMP§, AURELIA SIMONAVICIENE*, VITUS OBERHAUSER§, SABINE WESSELS*, STEPHAN R. ORTH{ddagger}, MARIE-LUISE GROSS*, ANDREAS KOCH*, GERHARD W. BIELENBERG||, JORGE P. VAN KATS, HEIMO EHMKE#, GERHARD MALL** and EBERHARD RITZ{ddagger}

* Department of Pathology, University of Heidelberg, Germany
{dagger} Department of Pathology, University of Erlangen-Nürnberg, Germany
{ddagger} Department of Internal Medicine, University of Heidelberg, Germany
§ Department of Internal Medicine IV, University of Freiburg, Germany
|| Solvay Pharma, Hannover, Germany
Department of Internal Medicine, Erasmus University, Rotterdam, The Netherlands
# Department of Physiology, University of Hamburg, Germany
** Department of Pathology, Darmstadt, Germany.

Correspondence to Dr. Kerstin Amann, Dept. of Pathology, University Erlangen-Nürnberg, Krankenhausstrasse 8-10, D-91054 Erlangen, Germany. Phone: +49 09131 85 22291; Fax: +49 09131 85 24745; E-mail: kerstin.amann{at}patho.imed.uni-erlangen.de

Abstract. A potential role of the sympathetic nervous system in progression of renal failure has received little attention. This study examined whether nonhypotensive doses of moxonidine, an agent that reduces sympathetic activity, affects glomerulosclerosis, urine albumin excretion, and indices of renal handling of norepinephrine (NE) in subtotally nephrectomized (SNX) rats. Sprague Dawley rats were SNX or sham-operated (control). SNX rats were either left untreated or treated with moxonidine in a dose (1.5 mg/kg body wt per d) that did not modify telemetrically monitored 24-h BP. Glomerular and renal morphology were evaluated by quantitative histology, immunohistochemistry, and in situ hybridization. Urine albumin excretion rate was analyzed by enzyme-linked immunosorbent assay, and kidney angiotensin II and NE content were measured using HPLC, 3H-NE uptake, and release. Body and kidney weight and BP were not significantly different between SNX with or without moxonidine. The glomerulosclerosis index was significantly lower in moxonidine-treated (0.88 ± 0.09) compared with untreated (1.55 ± 0.28) SNX rats, as was the index of vascular damage (0.32 ± 0.14 versus 0.67 ± 0.16). The number of proliferating cell nuclear antigen-positive glomerular and tubular cells per area was significantly higher in untreated SNX rats than in controls and moxonidine-treated SNX rats. The same was true for urine albumin excretion rate. Renal angiotensin II tissue concentration was not affected by moxonidine. In untreated SNX rats, renal nerve stimulation and exogenous NE induced an increase in isolated kidney perfusion pressure (102 ± 21 versus 63 ± 8 mmHg). Renal endogenous NE content was significantly lower in SNX rats than in controls (86 ± 14 versus 140 ± 17 pg/mg wet weight). Cortical uptake of [3H]-NE was not different, but cortical NE release was significantly higher in SNX rats than in controls. Reduced function of presynaptic inhibitory {alpha}-adreno-receptors is unlikely because an {alpha}2-adrenoceptor antagonist increased NE release. At subantihypertensive doses, moxonidine ameliorates renal structural and functional damage in SNX animals, possibly through central inhibition of efferent sympathetic nerve traffic. In kidneys of SNX rats, indirect evidence was found for increased activity of a reduced number of nerve fibers.




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