Site and mechanism of action of dynorphin A-(1–13) andN-methyl-d -aspartate on ACTH release in fetal sheep
Autor: | I. Ross Young, David W. Walker, Dunli Wu, Yi Soong, Hazel H. Szeto, Laura Nardo |
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Rok vydání: | 2002 |
Předmět: |
endocrine system
medicine.medical_specialty N-Methylaspartate Physiology Placenta Endocrinology Diabetes and Metabolism Indomethacin Hypothalamus Neuropeptide Dynorphin Adrenocorticotropic hormone Biology Dynorphins chemistry.chemical_compound Fetus Adrenocorticotropic Hormone Pregnancy Physiology (medical) Internal medicine medicine Animals Cyclooxygenase Inhibitors Receptor Sheep Receptors Opioid kappa 3 4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide (trans)-Isomer Dynorphin A respiratory system Peptide Fragments Endocrinology nervous system chemistry Mechanism of action Pituitary Gland embryonic structures NMDA receptor Female medicine.symptom hormones hormone substitutes and hormone antagonists |
Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 282:E1301-E1307 |
ISSN: | 1522-1555 0193-1849 |
DOI: | 10.1152/ajpendo.00527.2001 |
Popis: | Dynorphin A (Dyn A) stimulates the release of ACTH in fetal sheep, a response that involves N-methyl-d-aspartate (NMDA) receptors but not the secretogogues corticotropin-releasing hormone or arginine vasopressin. We now find that neither Dyn A-(1–13) (0.5 mg/kg, iv) nor NMDA (4 mg/kg, iv) elicits ACTH release in postnatal lambs. This led us to hypothesize that Dyn A-(1–13) and NMDA might act to release placental ACTH. However, the ability of Dyn A-(1–13), NMDA, and the κ-opioid receptor agonist U-50488H (1 mg/kg, iv) to release ACTH was lost after either fetal hypophysectomy ( n = 4) or hypothalamo-pituitary disconnection ( n = 4). These results indicate that neither the placenta nor the fetal pituitary is the site of action for these agonists and suggest a hypothalamic or suprahypothalamic site of action. Furthermore, the release of ACTH by Dyn A-(1–13) and NMDA was abolished after pretreatment with indomethacin, suggesting that they might cause the release of a prostanoid, possibly from the placenta, that subsequently acts at the hypothalamus or serves as a permissive factor in the action of Dyn A-(1–13) and NMDA at the hypothalamus. |
Databáze: | OpenAIRE |
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