Abstract P307: Renal Natural Killer Cell Activation and Mitochondrial Oxidative Stress; New Mechanisms in AT1-AA Mediated Hypertensive Pregnancy
| Autor: | Mark W Cunningham, Kristen McMaster, Tarek Ibrahim, Babbette LaMarca, Nathan Usry, Denise C. Cornelius, Lorena M. Amaral, Venkata Ramana Vaka, Gerd Wallukat, Shyanne McDuffy, R. Dechend, Nathan Campbell |
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| Rok vydání: | 2018 |
| Předmět: |
chemistry.chemical_classification
medicine.medical_specialty Reactive oxygen species Inflammation Mitochondrion medicine.disease_cause medicine.disease Angiotensin II Preeclampsia Endocrinology chemistry Internal medicine cardiovascular system Internal Medicine medicine medicine.symptom Receptor Natural killer cell activation hormones hormone substitutes and hormone antagonists Oxidative stress circulatory and respiratory physiology |
| Zdroj: | Hypertension. 72 |
| ISSN: | 1524-4563 0194-911X |
| DOI: | 10.1161/hyp.72.suppl_1.p307 |
| Popis: | Women with preeclampsia (PE) have increased blood pressure (MAP), natural killer (NK) cells, reactive oxygen species (ROS), and agonistic autoantibodies to the angiotensin II type 1 receptor (AT1-AA). AT1-AA’s administered to pregnant rodents produces a well-accepted model of PE. However, the role of NK cells and mitochondrial reactive oxygen species (mtROS) in AT1-AA mediated hypertension during pregnancy is unknown. We hypothesize that AT1-AA induced model of PE will exhibit elevated MAP, NK cells, and mtROS; while inhibition of the AT1-AA binding to the AT1R would be preventative. Pregnant rats were divided into 3 groups: normal pregnant (NP) (n=5), NP + AT1-AA infused (NP + AT1-AA) (n= 10), and NP + AT1-AA + AT1-AA inhibitory peptide (NP + AT1-AA + ‘n7AAc’) (n=8). Day 13, rats were surgically administered mini-pumps with either AT1-AA or AT1-AA+‘n7AAc’. Day 19, tissue and blood was collected. MAP was elevated in AT1-AA vs. NP (119±1 vs. 102±2 mmHg, pResearch Supported by NIH grants HL78147, HL51971, and HD067541 awarded to BL. DC is supported by NIH grant HL130456 and the American Heart Association 16SDG27520000. |
| Databáze: | OpenAIRE |
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