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Articles in PresS, published online ahead of print October 10, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00209.2001
Submitted on July 5, 2001
Accepted on September 26, 2001
1 Pharmacology, University of Regensburg, Regensburg, Germany
2 Physiology, University of Regensburg, Regensburg, Germany
3 Internal Medicine II, University of Regensburg, Regensburg, Germany
* To whom correspondence should be addressed. E-mail: klaus.hoecherl{at}chemie.uni-regensburg.de.
Salt deficiency induced by low salt diet in combination with inhibition of the renin angiotensin system leads to a stronger parallel increase of renin, cyclooxygenase-2 and neuronal NO-synthase gene expression in the juxtaglomerular apparatus of rat kidneys than low salt diet alone. Since the pathways that cause the marked concerted upregulation of the three genes are not well understood, we have investigated a possible involvement of the sympathetic nervous system in this context. We determined the effects of renal denervation as well as the effect of ß-adrenoreceptor antagonist (metoprolol 50 mg per kg body weight, p.o., twice a day) on renocortical expression of renin, COX-2 and nNOS in rats fed a low salt diet (0.02 % w/w) or treated for one week with the angiotensin-converting enzyme (ace) inhibitor ramipril (10 mg per kg body weight) in combination with low salt diet. We found that salt restriction by low salt diet and ace-inhibition strongly increased renocortical mRNA levels for renin, COX-2 and nNOS, 9-fold, 7-fold and 2.5 fold, respectively. Treatment with metoprolol did not change basal expression of the 3 genes nor the induction of renin and COX-2 gene expression by a low salt diet or in combination with ace-inhibition, whilst the induction of nNOS expression was clearly attenuated. Similarly, unilateral renal denervation attenuated the induction of nNOS expression, but left all other parameters unchanged. Renal cortical tissue concentrations of epinephrine, norepinephrine and dopamine were not changed during salt depletion. These findings suggest that ß-adrenergic stimulation is not required for the stimulation of renin and of COX-2 gene expression in the juxtaglomerular apparatus during salt deficiency. However, ß-adrenoreceptor activity or renal nerve activity appear to be required for the full stimulation of nNOS expression by low salt intake or combined with ace-inhibition.
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