腎素

腎素
	PDB rendering based on 2ren.
有效結構
PDB	直系同源檢索：PDBe, RCSB
PDB查詢代碼列表
	1BBS, 1BIL, 1BIM, 1HRN, 1RNE, 2BKS, 2BKT, 2FS4, 2G1N, 2G1O, 2G1R, 2G1S, 2G1Y, 2G20, 2G21, 2G22, 2G24, 2G26, 2G27, 2I4Q, 2IKO, 2IKU, 2IL2, 2REN, 2V0Z, 2V10, 2V11, 2V12, 2V13, 2V16, 2X0B, 3D91, 3G6Z, 3G70, 3G72, 3GW5, 3K1W, 3KM4, 3OAD, 3OAG, 3OOT, 3OQF, 3OQK
標識
代號	REN; FLJ10761; HNFJ2
擴展標識	遺傳學：179820 鼠基因：97898 同源基因：20151 GeneCards: REN Gene
EC編號	3.4.23.15
基因本體論描述
分子功能	· aspartic-type endopeptidase activity; · receptor binding; · insulin-like growth factor receptor binding; · peptidase activity;
細胞成分	· extracellular region; · extracellular space; · membrane; · cytoplasmic part;
生物過程	· kidney development; · mesonephros development; · angiotensin maturation; · proteolysis; · response to stress; · regulation of blood pressure; · male gonad development; · response to drug; · regulation of MAPKKK cascade; · response to cAMP; · response to cGMP;
	Sources: Amigo / QuickGO
直系同源體
	閱; 論; 編;

腎素（瑞典語、德語、英語：Renin），也被稱為血管緊張素原酶，是腎素-血管緊張素系統的組成部分。腎素最早於1898年由瑞典斯德哥爾摩卡羅琳學院生理學教授Robert Tigerstedt發現、描述並命名。

結構[編輯]

腎素前體由406個氨基酸殘基組成，包括分別包含20和46個氨基酸的前/後片斷。成熟的腎素包含340個氨基酸殘基，分子量為37kD。^[1]

分泌[編輯]

腎素由腎小球旁器的細胞經以下刺激分泌：

血壓下降
腎單位超濾液（原尿）中氯化鈉濃度下降
交感神經興奮

人的腎素分泌有至少兩條細胞途徑：分泌腎素原的結構途徑和分泌成熟腎素的經調解途徑。^[2]

功能[編輯]

腎素通過剪切肝臟合成的血管緊張素原產生血管緊張素I。血管緊張素I能進一步被血管緊張素轉化酶（Angiotensin Converting Enzyme, ACE）剪切成血管緊張素II。^[3]^[4] 血管緊張素II能夠高效地收縮血管，增加醛固酮和抗利尿激素分泌，刺激下丘腦產生渴覺，並最終升高血壓。

分泌腎素的顆粒細胞接受緻密斑（macula densa）細胞分泌的前列腺素刺激^[5]。而緻密斑能通過血管內的牽張感受器感知遠端小管流量下降，也能接受神經刺激（主要通過β-1腎上腺素能受體）。通過緻密斑的遠端小管流量下降反映了腎濾過壓的降低。而腎素的主要功能即是通過最終升高血壓來維持腎濾過壓^[6]。

參考文獻[編輯]

^ Imai T; Miyazaki H; Hirose S; et al. Cloning and sequence analysis of cDNA for human renin precursor. Proc. Natl. Acad. Sci. U.S.A. December 1983, 80 (24): 7405–9. PMC 389959 . PMID 6324167.
^ Pratt RE, Flynn JA, Hobart PM, Paul M, Dzau VJ. Different secretory pathways of renin from mouse cells transfected with the human renin gene. J. Biol. Chem. March 1988, 263 (7): 3137–41. PMID 2893797.
^ Fujino T; Nakagawa N; Yuhki K; et al. Decreased susceptibility to renovascular hypertension in mice lacking the prostaglandin I2 receptor IP. J. Clin. Invest. September 2004, 114 (6): 805–12 [2008-11-26]. PMC 516260 . PMID 15372104. doi:10.1172/JCI21382. （原始內容存檔於2012-02-22）.
^ Brenner & Rector's The Kidney, 7th ed., Saunders, 2004. pp.2118-2119.Full Text with MDConsult subscription （頁面存檔備份，存於網際網路檔案館）
^ Breyer MD, Breyer RM. Prostaglandin E receptors and the kidney. Am. J. Physiol. Renal Physiol. July 2000, 279 (1): F12–23.
^ Grendelmeier I. Renale Hypertonie – die Rolle der Nieren bei der Entstehung der arteriellen Hypertonie und die Nieren als Endorgan. Ther. Umsch. 2015-06, 72 (6): 369–74. doi:10.1024/0040-5930/a000688.

[1] Imai T; Miyazaki H; Hirose S; et al. Cloning and sequence analysis of cDNA for human renin precursor. Proc. Natl. Acad. Sci. U.S.A. December 1983, 80 (24): 7405–9. PMC 389959 . PMID 6324167.

[2] Pratt RE, Flynn JA, Hobart PM, Paul M, Dzau VJ. Different secretory pathways of renin from mouse cells transfected with the human renin gene. J. Biol. Chem. March 1988, 263 (7): 3137–41. PMID 2893797.

[3] Fujino T; Nakagawa N; Yuhki K; et al. Decreased susceptibility to renovascular hypertension in mice lacking the prostaglandin I2 receptor IP. J. Clin. Invest. September 2004, 114 (6): 805–12 [2008-11-26]. PMC 516260 . PMID 15372104. doi:10.1172/JCI21382. （原始內容存檔於2012-02-22）.

[4] Brenner & Rector's The Kidney, 7th ed., Saunders, 2004. pp.2118-2119.Full Text with MDConsult subscription （頁面存檔備份，存於網際網路檔案館）

[5] Breyer MD, Breyer RM. Prostaglandin E receptors and the kidney. Am. J. Physiol. Renal Physiol. July 2000, 279 (1): F12–23.

[6] Grendelmeier I. Renale Hypertonie – die Rolle der Nieren bei der Entstehung der arteriellen Hypertonie und die Nieren als Endorgan. Ther. Umsch. 2015-06, 72 (6): 369–74. doi:10.1024/0040-5930/a000688.

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