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      Vasopressin Release Induced by Water Deprivation: Effects of Centrally Administered Saralasin

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          Uncertainty exists as to whether endogenous angiotensin activates brain mechanisms controlling vasopressin (AVP) secretion during dehydration. We injected various doses of saralasin into a lateral cerebroventricle (IVT) of conscious, male rats deprived of water for 48 h and killed them at different times. The concentration of AVP in the plasma (p[AVP]), measured by radioimmunoassay, was unaffected by saralasin. IVT pretreatment with 1-Sar-8-Ile-angiotensin II blocked maximal AVP release by IVT angiotensin, but this pretreatment did not reduce p[AVP] after 24, 48 or 72 h water deprivation. A 3-hour continuous IVT infusion of CSF or saralasin (10 μg/h) into 48-hour water-deprived rats revealed equivalent p[AVP] and urine volumes. When the infusions were continued for 3 h more with water available, control and saralasin-treated rats: (a) drank at similar rates, (b) excreted similar amounts of urine, and (c) reduced their p[AVP] levels to the same extent. IVT saralasin did not affect p[AVP] of rats dehydrated with hypertonic NaCl. Combined IVT saralasin and atropine reduced p[AVP] of 48-hour water deprived rats about 30% (p < 0.05). We conclude that redundancy exists for sensing, integrating and releasing vasopressin in dehydrated rats.

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          Author and article information

          S. Karger AG
          27 March 2008
          : 37
          : 6
          : 401-405
          aBiomedical Research Division, NASA-Ames Research Center, Moffett Field, Calif., bPharmacology Department, College of Medicine, The Milton S. Hershey Medical Center of Pennsylvania State University, Hershey, Pa., USA
          123583 Neuroendocrinology 1983;37:401–405
          © 1983 S. Karger AG, Basel

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          Pages: 5
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