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      Synergistic effects of nitric oxide and prostaglandins on renal escape from vasopressin-induced antidiuresis.

      American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

      Aquaporin 2, Aquaporin 6, Aquaporins, biosynthesis, Diclofenac, pharmacology, Diuresis, drug effects, Drinking, Drug Synergism, Eating, Gene Expression Regulation, Kidney, metabolism, Male, NG-Nitroarginine Methyl Ester, Nitric Oxide, Nitric Oxide Synthase, Osmolar Concentration, Potassium, blood, Prostaglandin-Endoperoxide Synthases, Prostaglandins, Rats, Rats, Sprague-Dawley, Sodium, Time Factors, Urination, Vasopressins, Water-Electrolyte Balance, Animals

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          Recent results from our laboratories indicate that renal escape from AVP-induced antidiuresis is accompanied by marked downregulation of kidney aquaporin-2 (AQP2) and AVP V2 receptors. The present studies evaluated the effect of nitric oxide (NO) and 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 1 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 with the non-WL controls during all 5 days of WL. l-NAME (20 mg. kg(-1). day(-1)) 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(-1). day(-1)) or diclofenac (2.5 mg. kg(-1). day(-1)) did not significantly affect the escape phenomenon by itself, but the combination of l-NAME and diclofenac showed a marked inhibitory effect on the escape phenomenon, which was also 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 downregulate kidney AQP2 expression.

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