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      Effect of Serotonin on Vasopressin Release: A Comparison to Corticosterone, Prolactin and Renin

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          Previously we reported that 5 min after intracerebroventricular (i.c.v.) injection, serotonin (5-HT, 2.5 µg) produced increases in blood pressure and decreases in heart rate in conscious rats that were blocked by LY 53857 (a selective 5-HT<sub>2/1C</sub> antagonist) and were sensitive to vasopressin antagonism. The present studies were performed to determine if this dose of 5-HTacts similarly to increase plasma vasopressin levels. In addition, the vasopressin responses were compared to prolactin, corticosterone, and plasma renin activity, three other neuroendocrine systems regulated in part by 5-HT. The administration of 5-HT (2.5 µg i.c.v.) produced a rapid (maximum response in less than 5 min) and brief (return to baseline by 15 min) increase in plasma vasopressin levels. The response was eliminated by the centrally acting 5-HT2/1C antagonist LY 53857 (100 µg/kgi.v.), but only attenuated by xylamidine (100 µg/kg i.v.), a 5-HT<sub>2/1C</sub> antagonist that reportedly does not cross the blood-brain barrier. 5-HT also increased plasma prolactin and corticosterone levels, but neither LY 53857 nor xylamidine altered these responses. In rats rendered chronically baroreceptor deficient by sinoaortic deafferentation, the vasopressin response to 5-HT was reduced, whereas the prolactin response was normal. 5-HT did not increase plasma renin activity in intact or baroreceptor-deficient rats, in contrast to the other neuroendocrine systems studied. Thus, the data demonstrate that vasopressin levels are elevated briefly following 5-HTi.c.v., consistent with the pharmacologic profile of the early cardiovascular response. Although 5-HT<sub>2/1C</sub> receptors are implicated in both the vasopressin and cardiovascular responses, these same receptors do not exclusively mediate the prolactin or corticosterone responses to exogenous 5-HT.

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          Author and article information

          S. Karger AG
          08 April 2008
          : 57
          : 3
          : 550-558
          Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kans., USA
          126404 Neuroendocrinology 1993;57:550–558
          © 1992 S. Karger AG, Basel

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          Pages: 9
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