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1 NIDDK, National Institutes of Health,, Bethesda, Maryland, USA
2 NIDDK, National Institutes of Health,, Bethesda, Maryland, USA; Division of Nephrology, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA
* To whom correspondence should be addressed. E-mail: Tianxin.Yang{at}hsc.utah.edu.
It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are co-expressed in macula densa cells, and that the expression of both enzymes is stimulated in a number of high renin states. To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background, and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. In additional studies we accumulated evidence to show an inhibitory influence of PGE2 on nNOS expression. In a cultured macula densa cell line, PGE2 significantly reduced nNOS mRNA expression, as quantified by real-time RT-PCR. In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real time RT-PCR, was upregulated throughout the postnatal periods ranging from postnatal day (PND) 3 to PND 60. The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. Furthermore, the inhibitory effect of PGE2 on nNOS mRNA expression indicates a novel interaction between NO and prostaglandinsmediated pathways of renin regulation.
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