Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
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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 reabsorptionPurinergic signalling in the kidney in health and diseaseRenal autoregulation in health and diseaseRenal 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 miceThe proximal tubule in the pathophysiology of the diabetic kidney.Impaired glucose tolerance in the absence of adenosine A1 receptor signalingRenal 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 miceDense-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 diabetesRenal 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 ratsDiabetes-Induced Reactive Oxygen Species: Mechanism of Their Generation and Role in Renal InjuryPathophysiology 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.
P2860
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P2860
Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
@ast
Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
@en
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.
@en
prefLabel
Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
@ast
Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
@en
P2093
P2860
P356
P1476
Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
@en
P2093
Diane Mizel
Hiroshi Kajiyama
Jurgen Schnermann
Limeng Chen
Mona Oppermann
Noriyuki Hiramatsu
Patricia Zerfas
Robert Faulhaber-Walter
Soo Mi Kim
Yuning Huang
P2860
P304
P356
10.1681/ASN.2007060721
P577
2008-02-06T00:00:00Z