The role of cyclooxygenases and prostanoid receptorsin furosemide-like salt losing tubulopathy: the hyperprostaglandin E syndrome.

Abstract

Hyperprostaglandin E syndrome/antenatal Bartter syndrome is characterized by NaCl wasting and volume depletion, juxtaglomerula hypertrophy, hyperreninism and secondary hyperaldosteronism. Primary causes are mutations in the gene for Na-K-2Cl-cotransporter, NKCC2, or for potassium channel, ROMK, responsible for medullary NaCl malabsorption. Most intriguing aspect of the syndrome is the association with a massively increased renal prostaglandin production which contributes substantially to the clinical picture of the patients. Therefore the term hyperprostaglandin E syndrome has been introduced. It is unclear how prostaglandins aggravate the NaCl transport deficiency. Aspects to prostaglandin synthesis and receptor-mediated function within the kidney in patients suffering from hyperprostaglandin E syndrome/antenatal Bartter syndrome will be discussed.

• Authors: R M Nüsing, H W Seyberth
• Journal: Acta physiologica Scandinavica (Acta Physiol Scand) Vol. 181 Issue 4 Pg. 523-8 (Aug 2004) ISSN: 0001-6772 [Print] England
• PMID: 15283766 (Publication Type: Journal Article, Review)

Chemical References

• Prostaglandins E
• Receptors, Prostaglandin E
• Prostaglandin-Endoperoxide Synthases

Topics

• Bartter Syndrome (physiopathology)
• Diuresis
• Humans
• Kidney (metabolism)
• Prostaglandin-Endoperoxide Synthases (physiology)
• Prostaglandins E (biosynthesis)
• Receptors, Prostaglandin E (physiology)