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      Arginine Vasopressin Is a Much More Potent Stimulus to ACTH Release from Ovine Anterior Pituitary Cells than Ovine Corticotropin-Releasing Factor

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          Abstract

          Cultured rat and ovine anterior pituitary cells were treated with a range of doses (0.01–1,000 n M) of arginine vasopressin (AVP) and ovine corticotropin-releasing factor (CRF), alone or in combination, and medium and cell content of immunoreactive (ir-)ACTH determined. In rat cells, a dose-response curve to CRF was obtained, with a threshold dose of 0.1 n M; AVP was much less effective alone, but augmented CRF responses when administered with CRF. In ovine pituitary cells AVP markedly stimulated ACTH release in a dose-dependent fashion, and with a threshold of 0.1 n M; in contrast, CRF increased ACTH release over basal only at doses > 100 n M. In combination, subthreshold doses of AVP potentiated rat pituitary cell responses to CRF; addition of 1 n M of AVP to varying doses of CRF was more effective in terms of ACTH release than addition of 1 n M of CRF to increasing doses of AVP. In contrast, in ovine cells the addition of 1 n M CRF to increasing doses of AVP elicited a larger ACTH response than the addition of 1 n M AVP to increasing doses of CRF. Dexamethasone pretreatment (5 n M) for 48 h significantly decreased CRF potentiation of AVP-stimulated ACTH release in ovine cells. These studies confirm that CRF is a more potent stimulus of ACTH release than AVP in the rat, and establish that in contrast AVP is a much more potent stimulus of ACTH secretion than CRF in isolated ovine pituitary cells.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1989
          1989
          02 April 2008
          : 50
          : 2
          : 152-157
          Affiliations
          Medical Research Centre, Prince Henry’s Hospital, Melbourne, Australia
          Article
          125214 Neuroendocrinology 1989;50:152–157
          10.1159/000125214
          2550836
          © 1989 S. Karger AG, Basel

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          Page count
          Pages: 6
          Categories
          Original Paper

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