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Renal Medullary Interstitial COX-2 (Cyclooxygenase-2) Is Essential in Preventing
Salt-Sensitive Hypertension and Maintaining Renal Inner Medulla/Papilla
Structural Integrity.

Authors	Zhang MZ, Wang S, Wang Y, Zhang Y, Ming Hao C, Harris RC
Submitted By	Submitted Externally on 11/5/2018
Status	Published
Journal	Hypertension (Dallas, Tex. : 1979)
Year	2018
Date Published	11/1/2018
Volume : Pages	72 : 1172 - 1179
PubMed Reference	30354807
Abstract	COX (cyclooxygenase)-derived prostaglandins regulate renal hemodynamics and salt and water homeostasis. Inhibition of COX activity causes blood pressure elevation. In addition, chronic analgesic abuse can induce renal injury, including papillary necrosis. COX-2 is highly expressed in the kidney papilla in renal medullary interstitial cells (RMICs). However, its role in blood pressure and papillary integrity in vivo has not been definitively studied. In mice with selective, inducible RMIC COX-2 deletion, a high-salt diet led to an increase in blood pressure that peaked at 4 to 5 weeks and was associated with increased papillary expression of AQP2 (aquaporin 2) and ENac (epithelial sodium channel) and decreased expression of cystic fibrosis transmembrane conductance regulator. With continued high-salt feeding, the mice with RMIC COX-2 deletion had progressive decreases in blood pressure from its peak. After return to a normal-salt diet for 3 weeks, blood pressure remained low and was associated with a persistent urinary concentrating defect. Within 2 weeks of institution of a high-salt diet, increased apoptotic RMICs and collecting duct cells could be detected in papillae with RMIC deletion of COX-2, and by 9 weeks of high salt, there was a striking loss of the papillae. Therefore, RMIC COX-2 expression plays a crucial role in renal handling water and sodium homeostasis, preventing salt-sensitive hypertension and maintaining structural integrity of papilla.

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