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血管紧张素II(AT-2)多肽
产品名称:
血管紧张素II(AT-2)多肽
英文名称:
Angiotensin II Peptide
产品类别:
蛋白多肽
产品编号:
Y-0274
保存条件:
Shipped at 4℃. Stored at -20℃ for one year. Avoid
[价格]
规格 价格 库存
500ug ¥ 880.00 10

产品详情

产品编号Y-0274
英文名称Angiotensin II Peptide
中文名称血管紧张素II(AT-2)多肽
别????名Alpha 1 antiproteinase, antitrypsin; Ang II; ANG III; Angiotensin I; Angiotensin II; Angiotensin III; Angiotensinogen; Angiotensinogen (serpin peptidase inhibitor, clade A member 8); ANHU; Pre angiotensinogen; Serine (or cysteine) proteinase inhibitor; Serpin A8; SERPINA8; AT-2; AT-II; ANGT_HUMAN; 4474-91-3;??
性????状Lyophilized powder
序????列DRVYIHPF
纯化方法HPLC
活性Not tested
保存条件Shipped at 4℃. Stored at -20℃ for one year. Avoid repeated freeze/thaw cycles.
注意事项This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
产品介绍As part of the renin-angiotensin-aldosterone-system (RAAS), angiotensin II raises blood pressure by vasoconstriction, increased aldosterone release by the adrenal zona glomerulosa, sodium and water reabsorption in the proximal tubular cells, and vasopressin secretion. The direct action of angiotensin II on surrounding vessel walls is facilitated by binding to the G-protein-coupled angiotensin II receptor type 1 (AT-1) on vascular smooth muscle cells, which stimulates Ca2+/calmodulin-dependent phosphorylation of myosin and causes smooth muscle contraction that results in vasoconstriction . The RAAS is ultimately regulated by a negative feedback effect of angiotensin II on renin production by the juxtaglomerular cells of the renal afferent arteriole. Unresuscitated septic shock associated with marked hypovolemia, extracellular fluid volume depletion, decreased cardiac output, low arterial blood pressure and decreased systemic vascular resistance causes an increase in renin secretion by the juxtaglomerular cells, resulting in elevated angiotensin II plasma levels and an increased secretion of aldosterone from the adrenal cortex. Angiotensin II binding to AT-1 receptors causes dose-dependent vasoconstriction of both afferent and efferent glomerular arterioles. The most pronounced effect of angiotensin II results on efferent arterioles, resulting in reduced renal blood flow and increased glomerular filtration pressure.

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