Vasopressin release induced by water deprivation - Effects of centrally administered saralasin

Uncertainty exists as to whether endogenous angiotensin activates brain mechanisms controlling vasopressin (AVP) secretion during dehydration. Various doses of saralasin were injected into a lateral cgrebroventricle (IVT) of conscious, male rats deprived of water for 48 h. The rats were killed 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 hr water deprivation. A 3-hour continuous IVT infusion of CSF or saralasin (10 micrograms/hour) into 48-hour water-deprived rats revealed equivalent p(AVP) concentration and urine volumes. When the infusions were continued for 3 h more with water available, control and saralasin-treated rats: (1) drank at similar rates, (2) excreted similar amounts of urine, and (3) reduced their p(AVP) concentration levels to the same extent. IVT saralasin did not affect p(AVP) concentration of rats dehydrated with hypertonic NaCl. Combined IVT saralasin and atropine reduced p(AVP) concentration of 48-hour water deprived rats about 30 percent (p less than 0.05). It is concluded that redundancy exists for sensing, integrating and releasing vasopressin in dehydrated rats.