Dysregulation of Renal Cyclooxygenase-2 in Rats with Lithium-induced Nephrogenic Diabetes Insipidus.
- Author:
Tae Hwan KWON
1
Author Information
- Publication Type:Original Article
- Keywords: Aquaporins; Cyclooxygenase-2; Lithium; Prostaglandins
- MeSH: Animals; Aquaporins; Cyclooxygenase 2*; Diabetes Insipidus, Nephrogenic*; Dinoprostone; Immunoblotting; Immunohistochemistry; Kidney; Lithium; Osmolar Concentration; Prostaglandins; Rats*
- From:Electrolytes & Blood Pressure 2007;5(2):68-74
- CountryRepublic of Korea
- Language:English
- Abstract: This study aimed to examine whether the expression of major prostaglandin E2 (PGE2) synthesis enzyme, cyclooxygenase-2 (COX-2), is changed in the kidneys of the rats with lithium-induced nephrogenic diabetes insipidus (Li-NDI). Sprague- Dawley rats treated with lithium for 4 weeks were used as the NDI model and expression of renal COX-2 was determined by immunoblotting and immunohistochemistry. In Li-NDI where urine output was markedly increased and urine osmolality was significantly decreased, COX-2 expression in the inner medulla was decreased (28% of control), while it increased 18-fold in the cortex and outer medulla. Consistent with this, labeling intensity of COX-2 in macula densa region was increased, whereas it was decreased in the interstitial cells in the inner medulla, indicating a differential regulation of COX-2 between the cortex and inner medulla in Li-NDI. Accordingly, urinary PGE2 excretion was significantly increased in Li-NDI. In conclusion, there is a differential regulation of COX-2 between cortex and inner medulla in Li- NDI and urinary PGE2 excretion is increased in Li-NDI, possibly due to an increased renal production. This may suggest that increased renal production of PGE2 could play a role in modulating water reabsorption in the renal collecting duct in Li-NDI.
