Effect of dietary protein on rat renin and angiotensinogen gene expression.

Rosenberg, Mark E.; Chmielewski, David; Hostetter, Thomas H.

doi:10.1172/jci114546

Cited by 77 publications

(27 citation statements)

References 34 publications

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“…Since reduction of dietary protein intake also downregulates renin transcription (61), it is tempting to speculate that a decrease in intrarenal ANG II concentration which in turn reduces RANTES expression is responsible for some of the immune-protective effects associated with protein restriction.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II stimulates expression of the chemokine RANTES in rat glomerular endothelial cells. Role of the angiotensin type 2 receptor.

Wolf¹,

Ziyadeh²,

Thaiss³

et al. 1997

J. Clin. Invest.

232

178

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Section: Discussionmentioning

confidence: 99%

Angiotensin II stimulates expression of the chemokine RANTES in rat glomerular endothelial cells. Role of the angiotensin type 2 receptor.

Wolf¹,

Ziyadeh²,

Thaiss³

et al. 1997

J. Clin. Invest.

232

178

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“…RNA extraction, Northern analysis, and hybridization against cDNA probes were performed as detailed by Rosenberg et al (15). The cDNAs to human heme oxygenase were obtained from Dr. Tyrrell (1 1), and the cDNAs to rat catalase and glutathione peroxidase were from Dr. Furata (16) and Dr. Yoshimura (17), respectively.…”

Section: Glycerol Model Ofrhabdomyolysis (Glycerol Acute Renalfailurementioning

confidence: 99%

Induction of heme oxygenase is a rapid, protective response in rhabdomyolysis in the rat.

et al. 1992

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Heme proteins such as myoglobin or hemoglobin, when released into the extracellular space, can instigate tissue toxicity. Myoglobin is directly implicated in the pathogenesis of renal failure in rhabdomyolysis. In the glycerol model of this syndrome, we demonstrate that the kidney responds to such inordinate amounts of heme proteins by inducing the heme-degradative enzyme, heme oxygenase, as well as increasing the synthesis of ferritin, the major cellular repository for iron. Prior recruitment of this response with a single preinfusion of hemoglobin prevents kidney failure and drastically reduces mortality (from 100% to 14%). Conversely, ablating this response with a competitive inhibitor of heme oxygenase exacerbates kidney dysfunction. We provide the first in vivo evidence that induction of heme oxygenase coupled to ferritin synthesis is a rapid, protective antioxidant response. Our findings suggest a therapeutic strategy for populations at a high risk for rhabdomyolysis. (J. Clin. Invest. 1992. 90:267-270.)

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“…Sustained high protein intake raises plasma renin activity and renin mRNA levels in the kidney (18,23,24). However, it is difficult to relate the renal vasodilatory effects of protein or AA to increased renin activity.…”

Section: Introductionmentioning

confidence: 99%

Evidence for renal kinins as mediators of amino acid-induced hyperperfusion and hyperfiltration in the rat.

Jaffa¹,

Vío²,

Silva³

et al. 1992

J. Clin. Invest.

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This study examined the role of tissue kallikrein and kinins in renal vasodilation produced by infusion of amino acids (AA). In rats fed a 9% protein diet for 2 wk, intravenous infusion of a 10% AA solution over 60-90 min reduced total renal vascular resistance and increased glomerular filtration rate (GFR) by 2540% and renal plasma flow (RPF) by 23-30% from baseline. This was associated with a two-to threefold increase in urinary kinin excretion rate. Acute treatment of rats with aprotinin, a kallikrein inhibitor, resulted in deposition of immunoreactive aprotinin in kallikrein-containing connecting tubule cells and inhibited renal kallikrein activity by 90%. Aprotinin pretreatment abolished the rise in urinary kinins and prevented significant increases in GFR and RPF in response to AA. In a second group of rats pretreated with a B2 kinin receptor antagonist, [DArg Hyp3, Thi"'8 D Phe71 bradykinin, AA infusion raised urinary kinins identically as in untreated controls, but GFR and RPF responses were absent. Aprotinin or the kinin antagonist produced no consistent change in renal function in rats that were not infused with AA. AA-induced increases in kinins were not associated with an increase in renal kallikrein activity. Notably, tissue active kallikrein level fell 50% in AA-infused rats.

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Effect of dietary protein on rat renin and angiotensinogen gene expression.

Abstract: Plasma renin activity varies with the level of dietary protein, being higher on a high protein diet. To

Cited by 77 publications

References 34 publications

Angiotensin II stimulates expression of the chemokine RANTES in rat glomerular endothelial cells. Role of the angiotensin type 2 receptor.

Angiotensin II stimulates expression of the chemokine RANTES in rat glomerular endothelial cells. Role of the angiotensin type 2 receptor.

Induction of heme oxygenase is a rapid, protective response in rhabdomyolysis in the rat.

Evidence for renal kinins as mediators of amino acid-induced hyperperfusion and hyperfiltration in the rat.

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