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1 Physiology and Pharmacology, University of Southern Denmark, DK-5000 Odense, Denmark
2 Anatomy, Charite, 13353 Berlin, Germany
3 Integrative Pharmacology, AstraZeneca R & D, MoIndal, Sweden
* To whom correspondence should be addressed. E-mail: bljensen{at}health.sdu.dk.
We asked whether cyclooxygenase (COX) activity controls the renin angiotensin system in the postnatal period. During kidney development, renin peaked at postnatal days 0-1 at the mRNA, tissue protein (RRC) and plasma concentration (PRC) levels, and was widely expressed along preglomerular vessels. PRC and renin mRNA expression was elevated until weaning in the fourth postnatal week, compared to adult rats. Renocortical COX-2 was restricted to Tamm-Horsfall protein-positive cells in the cTAL, and cortical COX-2 mRNA and protein expression was elevated along with PRC in the second and third postnatal weeks. In contrast, cortical COX-1 expression was constant, but medullary COX-1 expression increased 8-fold from the first to fourth postnatal week. A COX-2 selective blocker, parecoxib, and a non-selective blocker, indomethacin, given in a period with COX-2 induction from postnatal day 6-12, markedly decreased PRC, but not renin mRNA or RRC. Inhibition of angiotensin AT1 receptors by candesartan from postnatal day 1-5 increased COX-2 mRNA (2.5-fold), protein, and distribution, renin mRNA (7-fold) and PRC (20-70-fold), but had no influence on COX-1 mRNA. Thus, due to very low levels of expression, COX-2 is unlikely to be responsible for the birth peak of renin, but COX-2 activity supports renin secretion later in the suckling period. ANG II negatively feeds back on renocortical COX-2 expression in the first postnatal days with high activity of the renin system. We suggest that suckling in the rat is correlated to an enhanced, COX-2-mediated, secretory activity of renin-producing JG-cells.
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