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mPGES-1 deletion impairs diuretic response to acute water loading

¹Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah; and Departments of ²Physiology and ³Cellular Biology and Anatomy, Medical College of Georgia, and ⁴Medical Research Service, Veterans Affairs Medical Center, Augusta, Georgia

Submitted 8 August 2008 ; accepted in final form 13 February 2009

PGE₂ has an established role in renal water handling. The present study was undertaken to examine the role of microsomal prostaglandin E synthase-1 (mPGES-1) in the diuretic response to acute and chronic water loading. Compared with wild-type (+/+) controls, mPGES-1 –/– mice exhibited impaired ability to excrete an acute, but not chronic water load. In response to acute water loading, urinary PGE₂ excretion in the +/+ mice increased at 2 h, in parallel with increased urine flow. In contrast, the –/– mice exhibited a delayed increase in urinary PGE₂ excretion, coinciding with the stimulation of renal medullary mRNA expression of cytosolic prostaglandin E synthase but not mPGES-2. At baseline, renal aquaporin-2 (AQP2) expression in mPGES-1 –/– mice was enhanced compared with the +/+ control. In response to acute water loading, renal AQP2 expression in the +/+ mice was significantly reduced, and this reduction was blunted in the –/– mice. Despite striking changes in AQP2 protein expression, renal AQP2 mRNA in both genotypes largely remained unchanged. Overall, these data support an important role of mPGES-1 in provoking the diuretic response to acute water loading.

water loading; aquaporin-2; collecting duct; diuresis

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