gms | German Medical Science

Sympathetic activity is a risk factor in the progression of renal failure in hypertension. In how far sympathetic overactivity can induce renal damage without co-factors like high blood pressure is unknown. Hence, we tested the hypothesis that increased renal sympathetic nerve activity (RSNA) in rats after myocardial infarction (CHF) induces signs of renal structural damage 21 days after ligature of the intraventricular coronary artery.

Renal morphology was evaluated 3 weeks after coronary ligature by quantitative histology and immunohistochemistry assessing signs of inflammation, fibrosis and increased extracellular matrix components. To measure renal sympathetic activity control and rats with myocardial infarction underwent volume expansion (0.9% NaCL; 10% body weight over 30 min) to decrease directly recorded renal sympathetic nerve activity (RSNA). The protocol was repeated in renally denervated animals (DNX). Renal excretory function and renal perfusion were assessed.

In CHF rats with intact renal innervation an increased formation of collagen I occured as compared to CHF rats with DNX. No gross signs of strucutural alterations could be observed in CHF rats. Volume expansion induced a an impaired decrease pattern of RSNA in CHF rats implying an increased RSNA activity. The excretion of the volume load was impaired in CHF rats [71% * vers. 92% (DNX) or 103% (Control); * p<0.05], although renal perfusion (GFR & RPF) was unaltered suggesting a main effect of the increased sympathetic nerve activity in the tubulo-interstitial area.

In an animal model of myocardial infarction increased sympathetic nerve activity may induce slight tubulointerstitial alterations. This is also the area where putatively the main functional effect of increased sympathetic nerve activity in myocardial infarction occurs (tubular salt and water reabsorption). Hence increased sympathetic nerve activity likely induces structural alterations in the kidney independently of other co-factors.