2013 Fiscal Year Final Research Report
Mineralocorticoid receptor blockade attenuates proliferative changes in the rat pulmonary artery in monocrotaline-induced pulmonary hypertension
| Project/Area Number |
22591987
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatric surgery
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| Research Institution | Osaka Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TERASAKI Fumio 大阪医科大学, 医学部・内科学3, 准教授 (20236988)
TAKAI Shinji 大阪医科大学, 薬理学, 准教授 (80288703)
KISHI Kanta 大阪医科大学, 小児科学, 助教 (20408503)
MORI Yasuhiko 大阪医科大学, 小児科学, 助教 (20287345)
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| Co-Investigator(Renkei-kenkyūsha) |
OKUMURA Kenichi 大阪医科大学, 小児科学, 助教 (10349699)
HAMORI Kan 大阪医科大学, リハビリテーション医学, 助教 (90581207)
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| Project Period (FY) |
2010-04-01 – 2013-03-31
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| Keywords | 肺高血圧 / ミネラロコルチコイド受容体 / ミネラロコルチコイド受容体拮抗剤 / エプレレノン / 治療 |
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| Research Abstract |
The aim of this study was to investigate a role of mineralocorticoid receptor (MR) signaling in the arteriolar remodeling of pulmonary artery hypertension (PAH) by antagonizing MR.
PAH was induced by a single subcutaneous injection of monocrotaline in male rats. Animals were divided in two groups: one group treated with oral MR antagonist and the other received no medication. MR antagonist treatment ameliorated increased reduced RV function and hypertrophy caused by elevated peak RV pressure seen in the group with no medication. The treatment group showed significantly less medial wall thickness and muscularization of PA compared to the group with no medication. MR antagonist treatment resulted in significant reduction in the mRNA levels of the MR, angiotensin 2 type 1a receptor and transforming growth factor beta1 in the lungs, when compared to the group with no medication.
These results suggest that MR signaling plays a role in the proliferative vascular remodeling of PAH.
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Research Products
(4 results)
