Angiotensin II Type 2 Receptor Inhibits Prorenin Processing in Juxtaglomerular Cells
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- ICHIHARA Atsuhiro
- Department of Internal Medicine, Keio University School of Medicine
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- HAYASHI Matsuhiko
- Department of Internal Medicine, Keio University School of Medicine
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- HIROTA Nobuhisa
- Department of Internal Medicine, Keio University School of Medicine
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- OKADA Hirokazu
- Internal Medicine, Saitama Medical College
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- KOURA Yukako
- Department of Internal Medicine, Keio University School of Medicine
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- TADA Yuko
- Department of Internal Medicine, Keio University School of Medicine
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- KANESHIRO Yuki
- Department of Internal Medicine, Keio University School of Medicine
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- TSUGANEZAWA Hirohiko
- Department of Internal Medicine, Keio University School of Medicine
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- SARUTA Takao
- Department of Internal Medicine, Keio University School of Medicine
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Long-term treatment with an angiotensin II type 1 receptor blocker (ARB) has been shown to decrease the plasma renin activity (PRA) of hypertensive patients, whereas PRA remains elevated during angiotensin-converting enzyme inhibitor (ACEI) treatment. In the present study, we used rat juxtaglomerular (JG) cells to elucidate the mechanism(s) involved in the differential regulation of PRA between ARB and ACEI treatment. Addition of 100 nmol/l angiotensinogen (Aogen) to JG cells (n =6 primary cultures) significantly increased the medium angiotensin (Ang) II levels from 14±2 to 440±9 pg/ml and suppressed the renin secretion rate (RSR) from 39.6±5.4% to 6.3±1.8% without affecting active renin content (ARC) or total renin content (TRC). In the Aogen-treated cells, the ACEI, delapril hydrochloride (CV3317, 10μmol/l), significantly decreased the medium Ang II levels to 58±14 pg/ml and increased RSR to 39.8±4.1% without affecting ARC or TRC. The ARB, an active metabolite of candesartan cilexetil (CV11974, 10μmol/l), however, significantly increased the medium Ang II levels and RSR to 486±15 pg/ml and 40.9±9.8%, respectively, and decreased ARC from 63.2±6.8 to 21.6±3.6 ng of Ang I•h-1•million cells-1 without affecting TRC. The decreases in ARC of the Aogen+CV11974-treated cells (n =6 primary cultures) were inhibited by an Ang II type 2 receptor blocker, PD123319 (10μmol/l). JG cells (n =6 primary cultures) were also treated with an Ang II type 2 receptor agonist, CGP42212A (0.1μmol/l). CGP42212A significantly increased RSR from 38.2±1.6% to 49.7±4.7% and decreased ARC from 60.8±3.0 to 25.3±2.8 ng of Ang I•h-1•million cells-1 without affecting TRC. Addition of CV11974 did not alter the RSR, ARC, or TRC of the CGP42212A-treated cells; however, PD123319 abolished the effects of CGP42212A. These results indicate that, distinct from ACEIs, ARBs inhibit prorenin processing of JG cells through Ang II type 2 receptors. Long-term treatment with an ARB may decrease PRA in part by diminishing the storage of active renin in JG cells. (Hypertens Res 2003; 26: 915-921)
収録刊行物
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- Hypertension Research
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Hypertension Research 26 (11), 915-921, 2003
日本高血圧学会
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詳細情報 詳細情報について
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- CRID
- 1390282679697977344
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- NII論文ID
- 10011875881
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- NII書誌ID
- AA10847079
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- COI
- 1:CAS:528:DC%2BD2cXmvVShsA%3D%3D
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- ISSN
- 13484214
- 09169636
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- PubMed
- 14714584
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- 本文言語コード
- en
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- データソース種別
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- JaLC
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- PubMed
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- 使用不可