Increased formation of prostaglandin E 2 (PGE 2 ) is a key part of hyperprostaglandin E syndrome/antenatal Bartter syndrome (HPS/aBS), a renal disease characterized by NaCl wasting, water loss, and hyperreninism. Inhibition of PGE 2 formation by cyclo-oxygenase inhibitors significantly lowers patient mortality and morbidity. However, the pathogenic role of PGE 2 in HPS/aBS awaits clarification. Chronic blockade of the Na-K-2Cl co-transporter NKCC2 by diuretics causes symptoms similar to HPS/aBS and provides a useful animal model. In wild-type (WT) mice and in mice lacking distinct PGE 2 receptors (EP1 In summary, these findings demonstrate that the EP4 receptor mediates PGE 2 -induced renin secretion and that EP1, EP3, and EP4 receptors all contribute to enhanced PGE 2 -mediated salt and water excretion in the HPS/aBS model.
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