17-hydroxyprogesterone blunts the hypertensive response associated with reductions in uterine perfusion pressure in pregnant rats
| Autor: | Babbette LaMarca, Marc Parrish, Sharon D. Keiser, Lillian Fournier Ray, William A. Bennett, Edward Veillon, Kathy Cockrell, James N. Martin, Joey P. Granger |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Mean arterial pressure
medicine.medical_specialty Placenta Article Preeclampsia Ischemia Pregnancy Internal medicine 17 alpha-Hydroxyprogesterone Caproate Hydroxyprogesterones medicine Animals Placental Circulation Endothelin-1 Progesterone Congeners Tumor Necrosis Factor-alpha business.industry 17-alpha-Hydroxyprogesterone Obstetrics and Gynecology Interleukin medicine.disease Endothelin 1 Rats Endocrinology In utero Gestation Female business Endothelin receptor Perfusion |
| Zdroj: | American Journal of Obstetrics and Gynecology. 201:324.e1-324.e6 |
| ISSN: | 0002-9378 |
| DOI: | 10.1016/j.ajog.2009.05.054 |
| Popis: | Reduction in uteroplacental perfusion (RUPP) in pregnant rats is associated with hypertension, elevated cytokines, and activation of the endothelin (ET-1) system. Our objective was to determine whether the antiinflammatory properties of 17-alpha-hydroxyprogesterone caproate (17 OHP) reduce cytokine-stimulated vasoactive pathways that are associated with hypertension in response to placental ischemia.Mean arterial pressure (MAP), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, and renal ET-1 were measured in the following: pregnant controls, pregnant controls plus 17 OHP (6.6 mg/kg), RUPP rats, and RUPP rats plus 17 OHP.MAP increased 29 mm Hg in RUPP rats compared with pregnant controls (P.001), whereas in RUPP plus 17 OHP rats, MAP increased only 19 mm Hg (P.05). TNF-alpha and IL-6 increased 2- to 3-fold, respectively, in response to placental ischemia but was normalized in RUPP rats treated with 17 OHP. ET-1 increased 3-fold in RUPP rats but was markedly less in RUPP plus 17 OHP rats.17 OHP blunts hypertension associated with RUPP, possibly via suppression of cytokine-stimulated ET-1 activation. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect