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1 Pharmacology, Universität Regensburg, Regensburg, Germany
2 Regensburg, Germany; Physiology, Universität Regensburg, Regensburg, Germany
3 Physiology, Universität Regensburg, Regensburg, Germany
* To whom correspondence should be addressed. E-mail: klaus.hoecherl{at}chemie.uni-regensburg.de.
The role of COX-2 for the control of renin is still a matter of debate, since studies with COX-2 deficient mice or with COX-2 inhibitors produced conflicting findings. Therefore, we studied the effect of the COX-2 inhibitor SC-58236 on the regulation of the renin system in adult rat kidneys. Renocortical tissue levels and urinary excretion of PGE2 were reduced to 65% and 40% of control values after a single gavage of SC-58236 and did not further decrease upon prolonged treatment. Plasma renin activity (PRA) and renin mRNA levels began to decrease after 3 days and reached a constant level to about 60% of control values after five days of treatment. Isoproterenol or left renal artery clipping for two days increased PRA and renin mRNA to similar levels both in vehicle and SC-58236 treated rats after two days. Pre-treatment with SC-58236 for five days, however, reduced the absolute increase in PRA and renin mRNA levels. Notably, the relative increases were not different between vehicle and SC-58236 treated rats. Similar findings were observed for the stimulation of the renin system by angiotensin II inhibition and low salt intake. These findings indicate that COX-2 inhibition attenuates renin secretion and renin gene expression stimulated by a variety of parameters in proportion to the lowering of basal renin activity, whilst it does not interfere with the different stimulatory mechanism per se. As a consequence, it appears as if COX-2 activity relevantly determines the set point of the activity of the renin system in rat kidneys.
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