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This version published online on December 18, 2003
Endocrinology, doi:10.1210/en.2003-0903
A more recent version of this article appeared on March 1, 2004
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*VASOPRESSIN

Submitted on July 22, 2003
Accepted on December 4, 2003

Regulation of Cyclooxygenase Expression by Vasopressin in Rat Renal Medulla

Ming-Zhi Zhang1, Pedro Sanchez Lopez1, James A. McKanna1, and Raymond C. Harris1*

1 George O'Brien Center for Kidney and Urologic Diseases, and Departments of Cell and Developmental Biologyand Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232

* To whom correspondence should be addressed. E-mail: ray.harris{at}vanderbilt.edu.

The antagonism between prostaglandin and vasopressin represents a classic negative feedback loop. It is not clear whether cyclooxygenase-2 (COX-2) and/or COX-1 expression are involved in elevated prostaglandin production stimulated by vasopressin in vivo. In the present study, we explored vasopressin regulation of medullary COX-2 and COX-1 expression acutely and chronically in rats. Medullary COX-1 expression was moderately and COX-2 expression was significantly lower in adult male Brattleboro rats than age-matched Long-Evans controls. Chronic treatment of Brattleboro rats with vasopressin for a week led to a decrease in urine volume and a moderate increase in medullary COX-1; in contrast, medullary COX-2 expression was almost undetectable in untreated rats but was dramatically upregulated with vasopressin treatment and was accompanied by increased urinary PGE2 excretion. Further investigation revealed that both V1 and V2 receptors were involved in chronic medullary COX-1 and COX-2 up-regulation. Acute treatment with specific V1 or V2 receptor agonists resulted in specific increases in medullary COX-2, which was prevented by furosemide. Vasopressin did not affect COX-2 expression in cultured renomedullary interstitial cells. These data demonstrate that vasopressin stimulates medullary COX-2 expression through activation of both V1 and V2 receptors, and this stimulation is indirect and probably involves increased medullary electrolyte tonicity.




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