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Institut für 1 Physiologie I and 4 Pharmakologie, Universität Regensburg, D-93040 Regensburg; 2 Nephrologie/Medicine Klinik IV, Universität Erlangen-Nürnberg, D-91054 Erlangen; 3 IMB, Afdeling for Fysiologi, DK-5000 Odense C; 6 Institut für Pharmakologie, Universität Regensburg, D-93040 Regensburg and 5 Innere Medicine II, Universitätsklinikum Regensburg, D-93053 Regensburg
This
study aimed to characterize the influence of acute renal artery
stenosis on cyclooxygenase-2 (COX-2) and renin expression in the
juxtaglomerular apparatus. For this purpose, male Sprague-Dawley rats
received a left renal artery clip, and COX-2 mRNA, COX-2 immunoreactivity, plasma renin activity, and renin mRNA levels were
determined. COX-2 mRNA and COX-2 immunoreactivity in the macula densa
region in the clipped kidneys increased as early as 6 h after
clipping and reached a maximal expression 1-2 days after clipping.
Although values for plasma renin activity were elevated markedly at all
time points examined, remaining renin mRNA levels were unchanged after
6 h and then increased to reach a maximum value 1-2 days
after clipping. In the contralateral intact kidney, renin mRNA and
COX-2 immunoreactivity decreased to ~50% of their normal values. To
investigate a possible causal relationship between the changes of COX-2
and of renin expression, clipped rats were treated with the COX-2
blocker celecoxib (40 mg · kg
1 · day1). This
treatment, however, did not change renin mRNA either in the clipped or
in the contralateral intact kidney. Our findings indicate that renal
artery stenosis causes ipsilaterally an acute upregulation and
contralaterally a downregulation of juxtaglomerular COX-2 expression.
The lacking effect of celecoxib on renin gene expression does not
support the concept of a direct mediator function of COX-2-derived
prostaglandins in the control of renin expression during renal hypoperfusion.
cycoloxygenase-1; cyclooxygenase-2; juxtaglomerular apparatus; renin ; prostaglandins; celecoxib
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