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Articles in PresS, published online ahead of print October 10, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00065.2002
Submitted on February 4, 2002
Accepted on October 8, 2002
1 Division of Endocrinology and Metabolism, Gerogetown University, Washington, DC, USA; Division of Endocrinology and Metabolism, Gerogetown University, Washington, DC, USA
2 Division of Endocrinology and Metabolism, Gerogetown University, Washington, DC, USA
3 Division of Nephrology and Hypertension, Gerogetown University, Washington, DC, USA
* To whom correspondence should be addressed. E-mail: verbalis{at}georgetown.edu.
Recent results from our laboratories indicate that renal escape from vasopressin (AVP)-induced antidiuresis is accompanied by marked down-regulation of kidney aquaporin-2 (AQP2) and AVP V2 receptors. The present studies evaluated the effect of nitric oxide (NO) and prostaglandins (PG) synthesis blockade on escape from antidiuresis. DDAVP-infused rats were water loaded (WL) for 5 days. L-NAME, an NO synthesis inhibitor, or diclofenac, a cyclooxygenase inhibitor, was infused subcutaneously beginning one day before WL. As early as 2 days after WL, urine volume increased and urine osmolality decreased, indicating the onset of escape. Endogenous NO synthesis, measured as urinary NO2 + NO3 excretion, was significantly increased in the WL group compared to the non-WL controls during all 5 days of WL. L-NAME (20 mg/kg/day) markedly decreased urine volume on days 4 and 5 of WL, indicating inhibition of the escape phenomenon. Kidney AQP2 protein was significantly increased by this dose of L-NAME as well. A lower dose of L-NAME (10 mg/kg/day) or diclofenac (2.5 mg/kg/day) did not significantly affect the escape phenomenon by themselves, but the combination of L-NAME and diclofenac showed a marked inhibitory effect on the escape phenomenon, which also was accompanied by a significant increase in kidney AQP2 expression. These results therefore suggest that renal NO and PG both play important roles in escape from AVP-induced antidiuresis by acting synergistically to down-regulate kidney AQP2 expression.
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