Key result
Deficiency of either COX-2 or nNOS in mice significantly reduced plasma renin activity, and PGE2 inhibited nNOS mRNA expression in macula densa cells.
Population
nNOS -/- mice on a mixed genetic background, COX-2 -/- mice on BALB/c or C57/BL6 congenic backgrounds, and a…
Comparison
Genetic knockout of nNOS or COX-2; PGE2… vs Wild-type controls (implied)
Design
Preclinical
Authors
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Hypothesis-generating for COX-2/nNOS renin interplay in mice; leaves open human relevance and should not change practice.
The absence of COX-2 or nNOS suppresses renin secretion, and PGE2 inhibits nNOS expression, indicating a novel interaction between NO and prostaglandin pathways in renin regulation.
Paliege et al. (2004) studied this question. nNOS or COX-2 deficiency and PGE2 exposure vs. Wild-type or control was evaluated on Plasma renin activity and nNOS mRNA expression. Deficiency of either COX-2 or nNOS in mice significantly reduced plasma renin activity, and PGE2 inhibited nNOS mRNA expression in macula densa cells.
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