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      Effects of Sodium Valproate and Diazepam on Beta-Endorphin, Beta-Lipotropin and Cortisol Secretion Induced by Hypoglycemic Stress in Humans

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          Abstract

          Evidence that γ-aminobutyric acid (GABA) and benzodiazepine receptors play a role in the inhibition of ACTH-cortisol secretion in humans has until now been drawn only from data indicating that sodium valproate, a GABA mimetic, and diazepam, a benzodiazepine, decrease hypothalamus-pituitary-adrenal (HPA) axis secretion in patients affected by pathological hypersecretion of the axis. Therefore, the present study investigated the effects, in the same healthy subjects, of sodium valproate or diazepam, on both basal and stress-stimulated concentrations of β-endorphin (β-EP), β-lipotropin (β-LPH) and cortisol. A single maximal dose of sodium valproate (400 mg) or diazepam (10 mg) did not significantly modify basal concentrations of β-EP, β-LPH and cortisol. On the other hand, in the same subjects, pretreatment with sodium valproate (20 mg × 3) or diazepam (10 mg × 2) blocked the increases in these hormones produced by hypoglycemic stress in all patients tested (p< 0.01 vs. placebo at 45, 60 and 90 min after insulin injection), without affecting the decrease in blood glucose levels. The present data show that sodium valproate and diazepam inhibit stress-induced β-EP, β-LPH and cortisol secretion in humans, suggesting that endogenous GABA and benzodiazepine receptors participate in physiological mechanisms regulating the activity of the HPA axis.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1986
          1986
          01 April 2008
          : 44
          : 3
          : 320-325
          Affiliations
          aDepartment of Obstetrics and Gynecology, University of Modena, School of Medicine, Modena, and bDepartment of Pharmacology, University of Milan, School of Medicine, Milan, Italy
          Article
          124663 Neuroendocrinology 1986;44:320–325
          10.1159/000124663
          3027601
          © 1986 S. Karger AG, Basel

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          Page count
          Pages: 6
          Categories
          Original Paper

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