| Project/Area Number |
04670537
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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 | Okayama University |
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Principal Investigator |
OGURA Toshio Third Dept of Int Med, Okayama Univ Med School, Lecturer, 医学部・附属病院, 講師 (80214097)
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| Co-Investigator(Kenkyū-buntansha) |
KASHIHARA Naoki Third Dept Int Med, Okayama Univ Med School, Assistant, 医学部・附属病院, 助手 (10233701)
MAKINO Hirofumi Third Dept Int Med, Okayama Univ Med School, Associated professor, 医学部, 助教授 (50165685)
HIRAKAWA Syuzo Third Dept Int Med, Okayama Univ Med School, Lecturer, 医学部・附属病院, 講師 (60156651)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1992: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | angiotensin II / c-fos / growth factor / spontaneously hypertensive rat / DOCA-salt hypertensive rat / vasopressin / dopamine / angiotensin converting enzyme inhibitor (ACEI) / バソプレッシン / PCR / 腎臓 / ACE阻害薬 / PDGF |
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| Research Abstract |
To elucidate the role or renin-angiotensin system (RAS) on blood pressure regulation and renal proliferation, we investigated the histological change or expression of growth factors from glomerulus in spontaneously hypetensive rat (SHR) and DOCA-salt hypertensive rat (DOCA). We also examined the effect of treatment with ACE inhibitor and AT1 receptor antagonist on the protection for hypertensive renal injury. It is resulted that RAS inhibition attenuate the expression of PDGFB-chain expression from glomerulus and improve the renal proliferative change, suggesting that the treatment with ACE inhibitor or AT1 receptor antagonist has beneficil effects to protect hypertensive nephropathy, clinically. Next, to elucidate the interaction between vasopressin (VP) system and blood pressure regulation, we investigated the acute pressor response under administration with VP,OPC-21268 (V1 receptor antagonist), OPC-31260 (V2 receptor antagonist) or combination of these agents in anesthetized SHR and DOCA.SHR had enhanced pressor response in the V1 stimulation, whereas DOCA had no such effect. These data demonstrate that SHR has a hypersensitivity state of V1 receptor, suggesting that V1 receptor may involve in the high blood pressure in SHR and VP system may not be important for blood pressure in DOCA.We also invesstigated the density of renal V1 and V2 receptors in SHR and DOCA using the quantification for in vitro macro-autoradiography. Although both renal V1 and V2 receptors in SHR increased with the elevation of blood pressure, renal VP receptors in DOCA decreased. We suggest that the elevation of blood pressure via high density of V1 receptors participate in the high blood pressure in SHR and that the renal VP receptors were down-regulated in DOCA whose blood VP concentration suppresed. These data seemed to be agree with the above-mentioned data in acute experiments.
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