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WATER AND ELECTROLYTE HOMEOSTASIS

Female ROMK null mice manifest more severe Bartter II phenotype on renal function and higher PGE₂ production

Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut

Submitted 24 January 2007 ; accepted in final form 21 June 2008

ROMK null mice with a high survival rate and varying severity of hydronephrosis provide a good model to study type II Bartter syndrome pathophysiology (26). During the development of such a colony, we found that more male than female null mice survived, 58.7% vs. 33.3%. To investigate the possible mechanism of this difference, we compared the survival rates, renal functions, degree of hydronephrosis, as well as PGE₂ and TXB₂ production between male and female ROMK wild-type and null mice. We observed that female ROMK Bartter's mice exhibited lower GFR (0.37 vs. 0.54 ml·min^–1·100 g BW^–1, P < 0.05) and higher fractional Na⁺ excretion (0.66% vs. 0.48%, P < 0.05) than male Bartter's. No significant differences in acid-base parameters, urinary K⁺ excretion, and plasma electrolyte concentrations were observed between sexes. In addition, we assessed the liquid retention rate in the kidney to evaluate the extent of hydronephrosis and observed that 67% of male and 90% of female ROMK null mice were hydronephrotic mice. Urinary PGE₂ excretion was higher in both sexes of ROMK null mice: 1.35 vs. 1.10 ng/24 h in males and 2.90 vs. 0.87 ng/24 h in females. TXB₂ excretion was higher in female mice in both wild-type and ROMK null mice. The increments of urinary PGE₂ and TXB₂ were significantly higher in female null mice than males, 233.33% vs. 22.74% of PGE₂ and 85.67% vs. 20.36% of TXB₂. These data demonstrate a more severe Bartter phenotype in female ROMK null mice, and higher PGE₂ and TXB₂ production may be one of the mechanisms of this manifestation.

gender difference; ROMK Bartter's; hydronephrosis; renal function