1995 Fiscal Year Final Research Report Summary
Angiotensin II receptor gene expression in the hypertensive endorgan damages and the effect of the treatment.
| Project/Area Number |
05670617
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Ehime University School of Medicine |
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Principal Investigator |
KOHARA Katsuhiko Ehime Univ 2nd Dept Intern Med, Lecturer, 医学部・附属病院, 講師 (30260384)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIDA Wataru School of Medicine, Ehime Univ.Assistant Professor, 医学部・附属病院, 助手 (80271089)
ABURAYA Masahito School of Medicine, Ehime Univ.Assistant Professor, 医学部・附属病院, 助手 (00260688)
OKURA Takafumi School of Medicine, Ehime Univ.Assistant Professor, 医学部・附属病院, 助手 (40260385)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Angiotensin II / Receptor / AT1 receptor subtype / AT2 receptor / SHR / Left Ventricular Hypertrophy / AT1 receptor antagonist / ACE inhibitor |
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| Research Abstract |
The levels of AT1A and AT1B receptor mRNA expression were evaluated by RT-PCR in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). At the age of 16-week old, there was no difference in AT1 receptor subtypes expression in the heart, adrenal gland or kidney between SHR and WKY except for the aorta in which AT1B was less expressed in SHR.
Antihypertensive treatment with either AT1 receptor antagonist or ACE inhibitor resulted in regression of left ventricular hypertrophy in SHR.After one week of the treatment, At1 receptor antagonist significantly decreased both AT1A and AT1B receptor mRNA expression, and ACE inhibitor significantly increased the levels of AT1A mRNA in the left ventricle of SHR.However, after four week of the treatment with both AT1 receptor antagonist and ACE inhibitor, the levels of AT1A and AT1B mRNA were returned to the control levels.
Using newly developed method, we evaluated the AT2 gene expression in rat adrenal gland. Bilateral nephrectomy as well as exogenous Ang II administration significantly increased the gene expression of AT2 mRNA in the rat adrenal gland. Althogh the property of AT2 receptor in the adrenal gland is still unknown, these findings indicate that alteration of the renin-angiotensin system can change the AT2 receptor gene expression.
Results obtained in the study indicate that Ang II receptor shows subtype specific changes in a tissue specific manner.
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