Renal Renin-Angiotensin System

Ichihara, Atsuhiro; Kobori, Hiroyuki; Nishiyama, Akira; Navar, L. Gabriel

doi:10.1159/000078716

Cited by 65 publications

(62 citation statements)

References 77 publications

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“…8). eNOS expression was increased at 4 weeks of diabetes, confirming our previous report (30) that it was reduced by telmisartan.…”

Section: Resultssupporting

confidence: 90%

“…This may be explained by an intrarenal system for renin (27), angiotensinogen (28), Ang II (29), and ACE (30) that is under regulation separate from juxtaglomerular renin release (28,30). Administration of an ACE inhibitor or an Ang II receptor blocker (ARB) to STZ-induced diabetic rats or patients with type 2 diabetes reduces markers of inflammation, oxidative stress, and albuminuria, independent of blood pressure or creatinine clearance (31,32).…”

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confidence: 99%

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Expression of NG,NG-Dimethylarginine Dimethylaminohydrolase and Protein Arginine N-Methyltransferase Isoforms in Diabetic Rat Kidney

et al. 2008

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OBJECTIVE-The nitric oxide (NO) synthase inhibitor asymmetric dimethylarginine (ADMA) is generated by protein arginine N-methyltransferase (PRMT)-1 and is metabolized by N G ,N Gdimethylarginine dimethylaminohydrolase (DDAH). We tested the hypothesis that increased serum ADMA (S ADMA ) in the streptozotocin (STZ)-induced diabetic rat model of diabetes is mediated by an angiotensin receptor blocker-sensitive change in DDAH or PRMT expression. RESEARCH DESIGN AND METHODS-Datawere compared from four groups of rats: sham-injected controls, untreated STZ-induced diabetic rats at 4 weeks, STZ-induced diabetic rats administered the angiotensin II (Ang II) receptor blocker telmisartan for 2 weeks, and control rats administered telmisartan for 2 weeks.RESULTS-Immunostaining and Western blotting of microdissected nephron segments localized DDAH I in the proximal tubules and DDAH II in the glomeruli, afferent arterioles, macula densa, and distal nephron. Renal Ang II and S ADMA increased with diabetes but were normalized by 2 weeks of telmisartan. DDAH I expression was decreased in diabetic kidneys, while DDAH II expression was increased. These changes were reversed by telmisartan, which also reduced expression of PRMT-1 and -5. Telmisartan increased expressions of DDAH I but decreased DDAH II in Ang II-stimulated kidney slices ex vivo. CONCLUSIONS-RenalAng II and S ADMA are increased in insulinopenic diabetes. They are normalized by an Ang II receptor blocker, which increases the renal expression of DDAH I, decreases PRMT-1, and increases renal NO metabolites.

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“…8). eNOS expression was increased at 4 weeks of diabetes, confirming our previous report (30) that it was reduced by telmisartan.…”

Section: Resultssupporting

confidence: 90%

mentioning

confidence: 99%

Expression of NG,NG-Dimethylarginine Dimethylaminohydrolase and Protein Arginine N-Methyltransferase Isoforms in Diabetic Rat Kidney

et al. 2008

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“…The importance of the intrarenal RAS in BP control is gaining increasing experimental support. Accumulating evidence suggests that activation of the RAS within the kidney, independent of the state of the systemic RAS, may induce Na retention and sustained hypertension (113). Despite that the intrarenal RAS is suppressed in the neonatal period in prenatally programmed hypertension in the rat, AT1R expression increases above control levels during the prehypertensive stage (97,114), without feedback suppression in kidney angiotensin I or II contents (97).…”

Section: Targets Of Programming In the Fetusmentioning

confidence: 99%

Prenatal Programming of Hypertension

Vehaskari¹,

Woods²

2005

Journal of the American Society of Nephrology

110

120

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“…Malignant hypertension is usually accompanied by a high secretion of renin by the kidney, which is not downregulated by the rise in blood pressure. In addition, local tissue angiotensin II is also activated in renal angiotensin-converting enzyme [29]. Angiotensin II contributes to systemic hypertension by constricting the efferent arterioles, causing an increase in intraglomerular pressure and filtration fraction.…”

Section: Discussionmentioning

confidence: 99%

A case of secondary focal segmental glomerulosclerosis associated with malignant hypertension

et al. 2012

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Focal segmental glomerulosclerosis (FSGS) is associated with various clinicopathological conditions, including hypertension. We report here a case of secondary FSGS associated with malignant hypertension. A 33-yearold man with a 1-month history of visual impairment and headache visited the Department of Ophthalmology at our hospital and was found to have hypertensive retinopathy and severe hypertension (230/160 mmHg). He was referred to our department based on suspected renal dysfunction. His blood pressure on admission was 250/130 mmHg. Physical examination and laboratory tests revealed hypertensive cardiac dysfunction, focal brain edema, renal dysfunction (serum creatinine, Cr 7.07 mg/dl, blood urea nitrogen, BUN 49.9 mg/dl), massive proteinuria (10.7 g/day), and thrombotic microangiopathy. Funduscopy showed exudate, hemorrhage, and papilledema. The cause of secondary hypertension could not be identified. He was treated for primary malignant hypertension, but required hemodialysis 3 days after admission due to anuria. Treatment with antihypertensive agents resulted in the gradual recovery of renal function, although heavy proteinuria continued with nephrotic syndrome. Renal biopsy performed 1 month after admission showed features of malignant nephrosclerosis with secondary FSGS. Hemodialysis was discontinued following further improvement in renal function and the most recent laboratory tests showed proteinuria 1.8 g/day and persistent renal dysfunction (BUN 36.5 mg/dl, Cr 3.14 mg/ dl). Malignant hypertension may cause various injuries, including glomerular endothelial and epithelial cell injuries in glomerular hypertension and hyperfiltration, increase of the renin-angiotensin-aldosterone system, and endothelialepithelial interaction, resulting in the development of secondary FSGS and heavy proteinuria.

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Renal Renin-Angiotensin System

Cited by 65 publications

References 77 publications

Expression of NG,NG-Dimethylarginine Dimethylaminohydrolase and Protein Arginine N-Methyltransferase Isoforms in Diabetic Rat Kidney

Expression of NG,NG-Dimethylarginine Dimethylaminohydrolase and Protein Arginine N-Methyltransferase Isoforms in Diabetic Rat Kidney

Prenatal Programming of Hypertension

A case of secondary focal segmental glomerulosclerosis associated with malignant hypertension

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