Angiotensin II type 1 receptor blockade opposes conduit artery endothelial dysfunction during no deficiency - Possible role of endothelium-derived hyperpolarizing factor

被引：0

作者：

Bellien, J. ^{[1
]}

Joannides, R. ^{[1
]}

Iacob, M. ^{[1
]}

Thuillez, C. ^{[1
]}

机构：

[1] Rouen Univ Hosp, Dept Pharmacol, INSERM, U644,IFRMP23, Rouen, France

来源：

JOURNAL OF HYPERTENSION | 2006年 / 24卷

关键词：

D O I：

暂无

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

引用

页码：S320 / S321

页数：2

共 35 条

[31] IL-17 causes hypertension and multi-organ tissue dysfunction which is attenuated with blockade of agonistic autoantibodies to the angiotensin II type I (AT1-AA) receptor during pregnancy
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[32] The role of T cell stimulated agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) in mediating multiorgan dysfunction in IL-17 induced hypertension during pregnancy
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[33] Angiotensin II type 1 receptor blockade by telmisartan prevents stress-induced impairment of memory via HPA axis deactivation and up-regulation of brain-derived neurotrophic factor gene expression
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[34] Extracellular signal-Regulated Kinase 1/2 is activated by angiotensin-II and pressure in rat mesenteric resistance arteries. A possible role for the platelet-derived growth factor-receptor.
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[35] A possible role for the platelet-derived growth factor-beta-receptor in angiotensin-II and pressure activation of extracellular signal-regulated kinase 1/2 in rat mesenteric arteries.
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