179 research outputs found
Mechanisms of progression of chronic kidney disease
Chronic kidney disease (CKD) occurs in all age groups, including children. Regardless of the underlying cause, CKD is characterized by progressive scarring that ultimately affects all structures of the kidney. The relentless progression of CKD is postulated to result from a self-perpetuating vicious cycle of fibrosis activated after initial injury. We will review possible mechanisms of progressive renal damage, including systemic and glomerular hypertension, various cytokines and growth factors, with special emphasis on the renin–angiotensin–aldosterone system (RAAS), podocyte loss, dyslipidemia and proteinuria. We will also discuss possible specific mechanisms of tubulointerstitial fibrosis that are not dependent on glomerulosclerosis, and possible underlying predispositions for CKD, such as genetic factors and low nephron number
Changes in levels of angiotensin II and its receptors in a model of inverted stress-induced cardiomyopathy
Intestinal intraepithelial lymphocyte derived angiotensin converting enzyme modulates epithelial cell apoptosis
Background & Aims : Intestinal adaptation in short bowel syndrome (SBS) consists of increased epithelial cell (EC) proliferation as well as apoptosis. Previous microarray analyses of intraepithelial lymphocytes (IEL) gene expression after SBS showed an increased expression of angiotensin converting enzyme (ACE). Because ACE has been shown to promote alveolar EC apoptosis, we examined if IEL-derived ACE plays a role in intestinal EC apoptosis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44361/1/10495_2005_Article_2138.pd
The subtype 2 angiotensin receptor regulates renal prostaglandin F2 alpha formation in conscious rats
The subtype 2 (AT2) angiotensin receptor mediates renal production of nitric oxide in conscious rats.
The subtype-2 (AT2) angiotensin receptor regulates renal cyclic guanosine 3', 5'-monophosphate and AT1 receptor-mediated prostaglandin E2 production in conscious rats.
Sustained hypersensitivity to angiotensin II and its mechanism in mice lacking the subtype-2 (AT2) angiotensin receptor
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