書誌事項
- タイトル別名
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- Pathophysiological significance of the natriuretic peptide system: receptor subtype as another key factor.
- ナトリウム リニョウ ペプチド ジュヨウタイ サブタイプ ノ ビョウタイ セイ
- 生体内活性物質研究の最先端
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The natriuretic peptide (NP) system is one of the most important systems regulating blood pressure and body-fluid homeostasis. The biological activities of the system are determined by the NPs and the receptors, which are comprised of three subtypes: NP-AR and NP-BR related to biological activities and NP-CR related to the clearance of NP. We focused our studies on the receptor subtypes. In hypertensive rats (SHR-SP/Izm, DOCA/salt), NP-AR was upregulated and NP-CR was downregulated. The ACE inhibitor derapril, but not the Ca2+ blocker manidipine, normalized the upregulated NP-AR, but the effect was completely abolished by the bradykinin β2- receptor antagonist, suggesting that bradykinin regulates the vascular NP-AR. The AT1 antagonist TCV-116, but not manidipine, reversed the downregulated NP-CR. Ang II decreased NP-CR in cultured aortic smooth muscle cells. These results suggest that upregulation of NP-AR and downregulation of NP-CR with the increased plasma NPs counteract hypertension by enhancing the action of NP. A β-blocker (carvedilol) potentiated the hypotensive action of NPs by increasing plasma NPs and enhancing the vascular response to NPs via downregulation of the vascular and lung NP-CR. The newly found mode of actions could be related to its anti-heart failure effect. In genetically hyperglycemic Wistar fatty rats, vascular NP-BR and NP-AR were upregulated. Since plasma ANP and vascular CNP were significantly increased, the local CNP/NP-BR system as well as the systemic ANP/NP-AR system may play an important role in counteracting vascular remodeling in diabetes mellitus. All these observations provide in vivo evidence for the pathophysiological significance of the receptor subtype of the NPs.
収録刊行物
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- 日本薬理学雑誌
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日本薬理学雑誌 112 (3), 147-154, 1998
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001204270988416
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- NII論文ID
- 10005086394
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- NII書誌ID
- AN00198335
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- COI
- 1:CAS:528:DyaK1cXlslKrsL4%3D
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- ISSN
- 13478397
- 00155691
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- NDL書誌ID
- 4549228
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- PubMed
- 9793068
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可
