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Angiotensin II receptor blocker/ja: Difference between revisions

Angiotensin II receptor blocker/ja
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Created page with "===線維症の退縮=== ロサルタンなどのARBは、筋肉、肝臓、心臓、腎臓の線維化を抑制または軽減することが示されている。"
 
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| [[Moderate sensitive substrate/ja|中程度のセンシティブ基質]]: [[CYP2C9/ja|CYP2C9]]
| [[Moderate sensitive substrate/ja|中程度のセンシティブ基質]]: [[CYP2C9/ja|CYP2C9]]


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|-
|-
| [[Valsartan]]
| [[Valsartan/ja|バルサルタン]]
| Diovan
| Diovan
| 6
| 6
| 2–4 hrs
| 2–4H
| 95%
| 95%
| 25%
| 25%
Line 147: Line 146:
| Yes
| Yes
| 80–320
| 80–320
| Substrates: [[Multidrug resistance-associated protein 2|MRP2]] and [[OATP1B1|OATP1B1/SLCO1B1]]
| 基質: [[Multidrug resistance-associated protein 2/ja|MRP2]]と[[OATP1B1/ja|OATP1B1/SLCO1B1]]
|-
|-
| [[Irbesartan]]
| [[Irbesartan/ja|イルベサルタン]]
| Avapro
| Avapro
| 11–15
| 11–15
| 1.5–2 hrs
| 1.5–2H
| 90–95%
| 90–95%
| 70%
| 70%
Line 158: Line 157:
| No
| No
| 150–300
| 150–300
| Minor substrates of [[CYP2C9]]
| [[CYP2C9/ja|CYP2C9]]のマイナー基質
|-
|-
| [[Telmisartan]]
| [[Telmisartan/ja|テルミサルタン]]
| Micardis
| Micardis
| 24
| 24
| 0.5–1 hr
| 0.5–1H
| >99%
| >99%
| 42–58%
| 42–58%
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| No
| No
| 40–80
| 40–80
| None known; >97% via biliary excretion
| 不明; >97% 胆汁排泄
|-
|-
| [[Eprosartan]]
| [[Eprosartan/ja|エプロサルタン]]
| Teveten
| Teveten
| 5
| 5
| 1–2 hrs
| 1–2H
| 98%
| 98%
| 13%
| 13%
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| No
| No
| 400–800
| 400–800
| None known; >90% via renal and biliary excretion
| 不明; >90% 腎と胆汁排泄
|-
|-
| [[Olmesartan]]
| [[Olmesartan/ja|オルメサルタン]]
| Benicar/Olmetec
| Benicar/Olmetec
| 14–16
| 14–16
| 1–2 hrs
| 1–2H
| >99%
| >99%
| 29%
| 29%
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| No
| No
| 10–40
| 10–40
| Substrates of [[OATP1B1|OATP1B1/SLCO1B1]]
| [[OATP1B1/ja|OATP1B1/SLCO1B1]]の基質
|-
|-
| [[Azilsartan]]
| [[Azilsartan/jaZ|アジルサルタン]]
| Edarbi
| Edarbi
| 11
| 11
| 1.5–3 hrs
| 1.5–3H
| >99%
| >99%
| 60%
| 60%
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| No
| No
| 40–80
| 40–80
| Minor substrates of CYP2C9
| CYP2C9のマイナー基質
|-
|-
| [[Fimasartan]]
| [[Fimasartan/ja|フィマサルタン]]
| Kanarb
| Kanarb
| 7–11
| 7–11
| 0.5–3 hrs after dosing.
| 服用後0.5–3H
| >97%
| >97%
| 30–40%
| 30–40%
Line 213: Line 212:
| –
| –
| 30–120
| 30–120
| None known; primarily biliary excretion
| 不明; 主に胆汁性排泄
|-
|-
! Drug
! 薬剤
! Trade name
! 製品名
! [[Biological half-life]] [hrs]
! [[Biological half-life/ja|半減期]] [時間]
! [[Cmax_(pharmacology)|Peak plasma concentration [Tmax] ]]
! [[Cmax_(pharmacology)/ja|ピーク血漿中濃度[Tmax]]]
! [[Protein binding]] [%]
! [[Protein binding/ja|タンパク質結合率]] [%]
! [[Bioavailability]] [%]
! [[Bioavailability/ja|生物学的利用能]] [%]
! Renal/hepatic [[Clearance (medicine)|clearance]] [%]
! 腎／肝[[Clearance (medicine)/ja|クリアランス]] [%]
! Food effect
! 食べ物の影響
! Daily dosage [mg]
! 容量/日 [mg]
! [[Metabolism]]/[[Transport protein|transporter]]
! [[Metabolism/ja|代謝]]/[[Transport protein/ja|トランスポーター]]
|}
|}
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{{further/ja|Discovery and development of angiotensin receptor blockers/ja}}
{{further|Discovery and development of angiotensin receptor blockers}}
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==研究==
==Research==
{{Anchor|Research}}
===Longevity===
===寿命===
Knockout of the Agtr1a gene that encodes AT<sub>1</sub> results in marked prolongation of the life-span of mice, by 26% compared to controls.  The likely mechanism is reduction of oxidative damage (especially to mitochondria) and overexpression of renal prosurvival genes. The ARBs seem to have the same effect.
AT<sub>1</sub>をコードするAgtr1a遺伝子をノックアウトすると、マウスの寿命は対照と比較して26％著しく延長する。 そのメカニズムとしては、酸化的損傷（特にミトコンドリア）の軽減と腎臓の生存促進遺伝子の過剰発現が考えられる。ARBにも同様の効果があるようだ。
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===線維症の退縮===
===Fibrosis regression===
ロサルタンなどのARBは、筋肉、肝臓、心臓、腎臓の線維化を抑制または軽減することが示されている。
ARBs, such as losartan, have been shown to curb or reduce muscular, liver, cardiac, and kidney fibrosis.
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===大動脈基部拡張の退縮===
===Dilated aortic root regression===
カンデサルタンとバルサルタンを用いた2003年の研究では、拡張した[[Ascending aorta/ja|大動脈起始部]]のサイズを退縮させる能力が示された。
A 2003 study using candesartan and valsartan demonstrated an ability to regress dilated [[Ascending aorta|aortic root]] size.
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==不純物==
==不純物==
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