Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury. - Wikidata - wikimedia - TriplyDB

Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

http://www.wikidata.org/entity/Q36666902

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C-Peptide: the missing link in diabetic nephropathy?Proinsulin C-peptide reduces diabetes-induced glomerular hyperfiltration via efferent arteriole dilation and inhibition of tubular sodium reabsorption Purinergic signalling in the kidney in health and disease Renal autoregulation in health and disease Renal failure in mice with Gsalpha deletion in juxtaglomerular cells.Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice.The renal vascular response to diabetes.Tubular reabsorption and diabetes-induced glomerular hyperfiltration.Maintained tubuloglomerular feedback responses during acute inhibition of P2 purinergic receptors in mice The proximal tubule in the pathophysiology of the diabetic kidney.Impaired glucose tolerance in the absence of adenosine A1 receptor signaling Renal hyperfiltration related to diabetes mellitus and obesity in human disease.Reduced Adenosine Uptake and Its Contribution to Signaling that Mediates Profibrotic Activation in Renal Tubular Epithelial Cells: Implication in Diabetic Nephropathy.Adenosine A1-receptor knockout mice have a decreased blood pressure response to low-dose ANG II infusion.Renal afferent arteriolar and tubuloglomerular feedback reactivity in mice with conditional deletions of adenosine 1 receptors.Tubuloglomerular feedback and renal function in mice with targeted deletion of the type 1 equilibrative nucleoside transporter.Direct assessment of tubuloglomerular feedback responsiveness in connexin 40-deficient mice.A High-throughput method for measurement of glomerular filtration rate in conscious mice.Salt sensitivity of blood pressure in NKCC1-deficient mice Dense-core vesicle proteins IA-2 and IA-2{beta} affect renin synthesis and secretion through the {beta}-adrenergic pathway.Role of glomerular filtration rate in controlling blood pressure early in diabetes Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney.Nephron filtration rate and proximal tubular fluid reabsorption in the Akita mouse model of type I diabetes mellitus.A selective EP4 PGE2 receptor agonist alleviates disease in a new mouse model of X-linked nephrogenic diabetes insipidus.Activation of adenosine receptors improves renal antioxidant status in diabetic Wistar but not SHR rats Diabetes-Induced Reactive Oxygen Species: Mechanism of Their Generation and Role in Renal Injury Pathophysiology of the diabetic kidney.Sodium-Glucose Cotransporter 2 Inhibitors with Renoprotective Effects.Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology.SGLT2 Protein Expression Is Increased in Human Diabetic Nephropathy: SGLT2 PROTEIN INHIBITION DECREASES RENAL LIPID ACCUMULATION, INFLAMMATION, AND THE DEVELOPMENT OF NEPHROPATHY IN DIABETIC MICE.Inhibition of sodium-linked glucose reabsorption normalizes diabetes-induced glomerular hyperfiltration in conscious adenosine A₁-receptor deficient mice.Retinal blood flow abnormalities following six months of hyperglycemia in the Ins2(Akita) mouse.High-protein-induced glomerular hyperfiltration is independent of the tubuloglomerular feedback mechanism and nitric oxide synthases.Activation of the renal renin-angiotensin system in diabetes--new concepts.Elucidating mechanisms underlying altered renal autoregulation in diabetes.The maturing relationship between tubules and glomeruli in diabetes mellitus.Salt-resistant blood pressure and salt-sensitive renal autoregulation in chronic streptozotocin diabetes.Differences in susceptibility to develop parameters of diabetic nephropathy in four mouse strains with type 1 diabetes.Insulin induces the correlation between renal blood flow and glomerular filtration rate in diabetes: implications for mechanisms causing hyperfiltration.Sodium glucose cotransporter 2 in mesangial cells and retinal pericytes and its implications for diabetic nephropathy and retinopathy.

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Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

http://www.wikidata.org/entity/Q36666902

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

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Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

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type

label

Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

@ast

Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

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prefLabel

Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

@ast

Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

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Journal of the American Society of Nephrology

P1476

Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.

@en

P2093

Diane Mizel

http://www.w3.org/2001/XMLSchema#string

Hiroshi Kajiyama

http://www.w3.org/2001/XMLSchema#string

Jurgen Schnermann

http://www.w3.org/2001/XMLSchema#string

Limeng Chen

http://www.w3.org/2001/XMLSchema#string

Mona Oppermann

http://www.w3.org/2001/XMLSchema#string

Noriyuki Hiramatsu

http://www.w3.org/2001/XMLSchema#string

Patricia Zerfas

http://www.w3.org/2001/XMLSchema#string

Robert Faulhaber-Walter

http://www.w3.org/2001/XMLSchema#string

Soo Mi Kim

http://www.w3.org/2001/XMLSchema#string

Yuning Huang

http://www.w3.org/2001/XMLSchema#string

P2860

Tubular sodium handling and tubuloglomerular feedback in experimental diabetes mellitus

Ornithine decarboxylase, kidney size, and the tubular hypothesis of glomerular hyperfiltration in experimental diabetes

Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes

A mutation in the insulin 2 gene induces diabetes with severe pancreatic beta-cell dysfunction in the Mody mouse

Mediation of tubuloglomerular feedback by adenosine: evidence from mice lacking adenosine 1 receptors

Senescence-associated phenotypes in Akita diabetic mice are enhanced by absence of bradykinin B2 receptors.

Kidney function in early diabetes: the tubular hypothesis of glomerular filtration.

Endothelial nitric oxide synthase deficiency produces accelerated nephropathy in diabetic mice.

Impairment of tubuloglomerular feedback regulation of GFR in ecto-5'-nucleotidase/CD73-deficient mice.

Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.

P304

722-730

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scholarly article

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10.1681/ASN.2007060721

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4

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P478

19

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Jeffrey B. Kopp

Josephine P Briggs

P577

2008-02-06T00:00:00Z

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5596573

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18256360

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2390969

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