Renal afferent denervation prevents the progression of renal disease in the renal ablation model of chronic renal failure in the rat

Rats with 5 6 nephrectomy develop hypertension and progressive deterioration in renal function. Several mechanisms may contribute to hypertension and to progressive renal disease in these rats. We have shown that increased activity of the sympathetic nervous system may contribute to hypertension in...

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Veröffentlicht in:American journal of kidney diseases 1995-11, Vol.26 (5), p.861-865
Hauptverfasser: Campese, Vito M., Kogosov, Ella, Koss, Michael
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Sprache:eng
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Zusammenfassung:Rats with 5 6 nephrectomy develop hypertension and progressive deterioration in renal function. Several mechanisms may contribute to hypertension and to progressive renal disease in these rats. We have shown that increased activity of the sympathetic nervous system may contribute to hypertension in rats with chronic renal failure. However, the role of the sympathetic nervous system activity in the progression of renal disease has not been investigated. We have evaluated whether neurogenic factors contribute to the progression of renal disease in the renal ablation model of chronic renal failure in the rat. Sprague-Dawley rats underwent 5 6 nephrectomy and dorsal rhizotomy or sham rhizotomy (CRF). Age-matched normal rats were used as controls. Six weeks after surgery, rats with chronic renal failure and dorsal rhizotomy had lower blood pressure and serum creatinine than rats with sham rhizotomy. In addition, kidneys from rats with 5 6 nephrectomy and rhizotomy manifested less severe glomerulosclerosis than kidneys from rats without dorsal rhizotomy. These studies have demonstrated that resection of renal afferent nerves prevents not only hypertension, but also the progression of renal disease in rats with renal ablation. Although normalization of blood pressure may definitely play a role, the data raise the possibility that neurogenic impulses to the kidneys may contribute to the progression of renal disease.
ISSN:0272-6386
1523-6838
DOI:10.1016/0272-6386(95)90456-5