血管緊張素是來源于血管緊張素原的小肽。幾種已知的血管緊張素是調節血壓的既定內分泌效應物，但它們也已知在一些器官和組織（旁分泌）和細胞水平（自分泌/內分泌）具有其他局部功能。血管緊張素I(DRVYIHPFHL)沒有已知的效應器功能，但它是血管緊張素II(DRVYIHPF)的直接前體。血管緊張素II與AT1受體結合，促進血管收縮、鈉潴留、醛固酮的釋放、氬加壓素的釋放、細胞增生、炎癥、纖維化、焦慮和心臟肥大。血管緊張素A(ARVYIHPF)，和血管緊張素III(RVYIHPF)，也與AT1受體結合。血管緊張素(1-7)(DRVYIHP)結合不同的受體，稱為MAS-1，具有相反的作用（血管擴張、利尿、抗擴散、NO釋放、PGE釋放和細胞凋亡）。血管緊張素IV(VYIHPF)與另一個稱為AT4(IRAP)的受體結合，促進血流增加、血管生成和利尿，它也與記憶的形成和阿爾茨海默病的發病機制有關。肽LVV-hemorphin-7（LVVYPWTQRF）不是血管緊張素，但也能與AT4受體結合。還有其他已經確定的血管緊張素肽，包括Ang(1-9)(DRVYIHPFH)、Ang(1-12)(DRVYIHPFHLVI)、Ang V(3-7)(VYIHP)，以及其他幾種功能未定的短肽。

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● 高度特異性，與類似肽交叉反應性低

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產品信息

部分產品引用文獻

1. ACE2-like enzyme B38-CAP suppresses abdominal sepsis and severe acute lung injury: T. Minato, et al.; PLoS One 17, e0270920 (2022)

2. Maternal perfluorooctane sulfonic acid exposure during rat pregnancy causes hypersensitivity to angiotensin II and attenuation of endothelium-dependent vasodilation in the uterine arteries: S.V. Dangudubiyyam, et al.; Biol. Reprod. 107, 1072 (2022)

3. Rapeseed (canola) oil aggravates metabolic syndrome-like conditions in male but not in female stroke-prone spontaneously hypertensive rats (SHRSP): M. Nishikawa, et al.; Toxicol. Rep. 9, 256 (2022)

4. Vasorin plays a critical role in vascular smooth muscle cells and arterial function: L. Louvet, et al.; J. Cell. Physiol. 237, 3845 (2022)

5. ACE2-like carboxypeptidase B38-CAP protects from SARS-CoV-2-induced lung injury: T. Yamaguchi, et al.; Nat. Commun. 12, 6791 (2021)

6. Advanced Oxidation Protein Product Promotes Oxidative Accentuation in Renal Epithelial Cells via the Soluble (Pro)renin Receptor-Mediated Intrarenal Renin-Angiotensin System and Nox4-H2O2 Signaling: K. Xue, et al.; Oxid. Med. Cell. Longev. 2021, 5710440 (2021)

7. The Expression of RAAS Key Receptors, Agtr2 and Bdkrb1, Is Downregulated at an Early Stage in a Rat Model of Wolfram Syndrome: M. Punapart, et al.; Genes (Basel) 12, 1717 (2021)

8. B38-CAP is a bacteria-derived ACE2-like enzyme that suppresses hypertension and cardiac dysfunction: T. Minato, et al.; Nat. Commun. 11, 1058 (2020)

9. Diabetes-induced Upregulation of Kallistatin Levels Exacerbates Diabetic Nephropathy via RAS Activation: Y. Yang, et al.; FASEB J. 34, 8428 (2020)

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