Blog
About

4
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      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

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          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.

          Related collections

          Author and article information

          Journal
          12388460
          10.1152/ajpregu.00065.2002

          Comments

          Comment on this article