| Hypertension in response to CD4(+) T cells from reduced uterine perfusion pregnant rats is associated with activation of the endothelin-1 system. | |
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MedLine Citation:
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PMID: 22647295 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We have shown that adoptive transfer of CD4(+) T cells from placental ischemia (reduction in uteroplacental perfusion, RUPP) rats causes hypertension and elevated inflammatory cytokines during pregnancy. In this study we tested the hypothesis that adoptive transfer of RUPP CD4(+) T cells was associated with endothelin-1 activation as a mechanism to increase blood pressure during pregnancy. CD4(+) T cells from RUPP or normal pregnant (NP) rats were adoptively transferred into NP rats on gestational day 13. Mean arterial pressure (MAP) was analyzed on gestational day 19, and tissues were collected for endothelin-1 analysis. MAP increased in placental ischemic RUPP rats versus NP rats (124.1 ± 3 vs. 96.2 ± 3 mmHg; P = 0.0001) and increased in NP recipients of RUPP CD4(+) T cells (117.8 ± 2 mmHg; P = 0.001 compared with NP). Adoptive transfer of RUPP CD4(+) T cells increased placental preproendothelin-1 mRNA 2.1-fold compared with NP CD4(+) T cell rats and 1.7-fold compared with NP. Endothelin-1 secretion from endothelial cells exposed to NP rat serum was 52.2 ± 1.9 pg·mg(-1)·ml(-1), 77.5 ± 4.3 pg·mg(-1)·ml(-1) with RUPP rat serum (P = 0.0003); 47.2 ± .16 pg·mg(-1)·ml(-1) with NP+NP CD4(+) T cell serum, and 62.2 ± 2.1 pg·mg(-1)·ml(-1) with NP+RUPP CD4(+) T cell serum (P = 0.002). To test the role of endothelin-1 in RUPP CD4(+) T cell-induced hypertension, pregnant rats were treated with an endothelin A (ET(A)) receptor antagonist (ABT-627, 5 mg/kg) via drinking water. MAP was 92 ± 2 mmHg in NP+ET(A) blockade and 108 ± 3 mmHg in RUPP+ET(A) blockade; 95 ± 5 mmHg in NP+NP CD4(+) T cells+ET(A) blockade and 102 ± 2 mmHg in NP+RUPP CD4(+) T cells+ET(A) blockade. These data indicate the importance of endothelin-1 activation to cause hypertension via chronic exposure to activated CD4(+) T cells in response to placental ischemia. |
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Authors:
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Kedra Wallace; Sarah Novotny; Judith Heath; Janae Moseley; James N Martin; Michelle Y Owens; Babbette LaMarca |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2012-05-30 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 303 ISSN: 1522-1490 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2012 Jul |
Date Detail:
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Created Date: 2012-07-16 Completed Date: 2012-10-02 Revised Date: 2013-05-06 |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R144-9 Citation Subset: IM |
Affiliation:
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Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, MS 39216, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adoptive Transfer Animals Blood Pressure / physiology CD4-Positive T-Lymphocytes / physiology*, transplantation Endothelin-1 / metabolism* Female Hypertension / physiopathology* Ischemia / physiopathology* Models, Animal Placenta / metabolism Pregnancy Pregnancy, Animal / physiology* Pyrrolidines / pharmacology RNA, Messenger / metabolism Rats, Sprague-Dawley Receptor, Endothelin A / antagonists & inhibitors, drug effects Signal Transduction / physiology Uterus / blood supply* |
| Grant Support | |
ID/Acronym/Agency:
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1F32HL-108558-01A1/HL/NHLBI NIH HHS; 1R01HD-067541-01A1/HD/NICHD NIH HHS; 1T32HL-105324/HL/NHLBI NIH HHS; F32 HL108558/HL/NHLBI NIH HHS; HL-51971/HL/NHLBI NIH HHS; R01 HD067541/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/A 127722; 0/Endothelin-1; 0/Pyrrolidines; 0/RNA, Messenger; 0/Receptor, Endothelin A |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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