The kallikrein-kinin and the renin-angiotensin systems have a multilayered interaction

Schmaier, Alvin H.

doi:10.1152/ajpregu.00535.2002

Cited by 150 publications

(134 citation statements)

References 150 publications

(182 reference statements)

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“…The expression of kallikrein decreased in the kidney after gentamicin (80 mg/kg/day, 7 days) ( Table 4). Kallikrein is a serine protease that cleaves kininogen to produce kinin, a vasoactive and natriuretic peptide (Clements 1989;Schmaier 2003). Kallikrein is produced and secreted in distal nephron segments and has been implicated in the control of sodium and water excretion and the long-term control of arterial pressure.…”

Section: Discussionmentioning

confidence: 99%

Identification of Putative Gene Based Markers of Renal Toxicity

Amin¹,

Vickers²,

Sistare³

et al. 2004

Environ. Health Perspect.

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This study, designed and conducted as part of the International Life Sciences Institute working group on the Application of Genomics and Proteomics, examined the changes in the expression profile of genes associated with the administration of three different nephrotoxicants-cisplatin, gentamicin, and puromycin-to assess the usefulness of microarrays in the understanding of mechanism(s) of nephrotoxicity. Male Sprague-Dawley rats were treated with daily doses of puromycin (5-20 mg/kg/day for 21 days), gentamicin (2-240 mg/kg/day for 7 days), or a single dose of cisplatin (0.1-5 mg/kg). Groups of rats were sacrificed at various times after administration of these compounds for standard clinical chemistry, urine analysis, and histological evaluation of the kidney. RNA was extracted from the kidney for microarray analysis. Principal component analysis and gene expression-based clustering of compound effects confirmed sample separation based on dose, time, and degree of renal toxicity. In addition, analysis of the profile components revealed some novel changes in the expression of genes that appeared to be associated with injury in specific portions of the nephron and reflected the mechanism of action of these various nephrotoxicants. For example, although puromycin is thought to specifically promote injury of the podocytes in the glomerulus, the changes in gene expression after chronic exposure of this compound suggested a pattern similar to the known proximal tubular nephrotoxicants cisplatin and gentamicin; this prediction was confirmed histologically. We conclude that renal gene expression profiling coupled with analysis of classical end points affords promising opportunities to reveal potential new mechanistic markers of renal toxicity.

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Section: Discussionmentioning

confidence: 99%

Identification of Putative Gene Based Markers of Renal Toxicity

Amin¹,

Vickers²,

Sistare³

et al. 2004

Environ. Health Perspect.

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show abstract

“…9,14 Since BK contributes to the antithrombotic nature of endothelium, we postulated that BKB2R KO (BKB2R Ϫ/Ϫ ) mice would be prothrombotic. 15 To our surprise we found that BKB2R Ϫ/Ϫ mice have long bleeding times and delayed thrombosis times due to an overexpressed angiotensin receptor 2 (AT 2 R) and elevated NO and prostacyclin levels. These investigations indicate a pathway for thrombosis risk reduction via the plasma kallikrein/kinin and renin angiotensin systems.…”

Section: Introductionmentioning

confidence: 93%

“…Synthesis of the first strand of cDNA was performed using 2 g to 5 g total RNA from heart, kidney, or liver of wild-type or BKB2R Ϫ/Ϫ mice as template and 1 L oligo(dT) [12][13][14][15][16][17][18] primer (500 g/mL), following the protocol accompanying the SUPERScript Preamplification System for First Strand cDNA Synthesis (Invitrogen). A 5-L aliquot of the cDNA synthesis reaction was amplified with 300 pmol of gene-specific oligonucleotide primers for the bradykinin B1 receptor (BKB1R; Gene Bank accession no.…”

Section: Cdna Synthesismentioning

confidence: 99%

Bradykinin B2 receptor knockout mice are protected from thrombosis by increased nitric oxide and prostacyclin

Shariat‐Madar

Mahdi

Warnock

et al. 2006

Blood

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103

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“…Normal kidney function is due to the proper balance between the KKS and the RAS (Schmaier, 2003). In addition, these systems are involved in renal development and maturation (Shen and El-Dahr, 2006).…”

Section: Renal Levels Of Vasoactive System Components Are Regulated Bmentioning

confidence: 99%

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

et al. 2012

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Acute renal failure (ARF) can be caused by injuries that induce tissue hypoxia, which in turn can trigger adaptive or infl ammatory responses. We previously showed the participation of basic fi broblast growth factor (FGF-2) in renal repair. Based on this, the aim of this study was to analyze the effect of FGF-2 signaling pathway manipulation at hypoxia-induced protein levels, as well as in key proteins from the vasoactive systems of the kidney. We injected rat kidneys with FGF-2 recombinant protein (r-FGF) or FGF-2 receptor antisense oligonucleotide (FGFR2-ASO) after bilateral ischemia, and evaluated the presence of iNOS, EPO and HO-1, in representation of hypoxiainduced proteins, as well as COX-2, renin, kallikrein, and B2KR, in representation of the vasoactive systems of the kidney. A reduction in iNOS, HO-1, EPO, renin, kallikrein, B2KR, and in renal damage was observed in animals treated with r-FGF. The opposite effect was found with FGF-2 receptor down-regulation. In contrast, COX-2 protein levels were higher in kidneys treated with r-FGF and lower in those that received FGFR2-ASO, as compared to saline treated kidneys. These res ults suggest that the protective role of FGF-2 in the pathogenesis of ARF induced by I/R is a complex process, through which a differential regulation of metabolic pathways takes place.

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The kallikrein-kinin and the renin-angiotensin systems have a multilayered interaction

Cited by 150 publications

References 150 publications

Identification of Putative Gene Based Markers of Renal Toxicity

Identification of Putative Gene Based Markers of Renal Toxicity

Bradykinin B2 receptor knockout mice are protected from thrombosis by increased nitric oxide and prostacyclin

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

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