Angiotensin-converting enzyme 2 mediates hyperfiltration associated with diabetes.

No abstract is available for this paper.

• Publication year

  2014

• Venue

  AJP - Renal Physiology

• Publication date

  2014-04-01

• Fields of study

  Medicine, Chemistry

• Identifiers
  DOI 10.1152/ajprenal.00264.2013PMID 24477684
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1-7) administration in anesthetized rats.

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• Acute and chronic effects of SGLT2 blockade on glomerular and tubular function in the early diabetic rat.

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• Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney.

  2012influential reference
• Interaction of diabetes and ACE2 in the pathogenesis of cardiovascular disease in experimental diabetes.

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• Insulin induces the correlation between renal blood flow and glomerular filtration rate in diabetes: implications for mechanisms causing hyperfiltration.

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• Anomalous role for dietary salt in diabetes mellitus?

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• High-protein-induced glomerular hyperfiltration is independent of the tubuloglomerular feedback mechanism and nitric oxide synthases.

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• Major role for ACE-independent intrarenal ANG II formation in type II diabetes.

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• Genetic Ace2 Deficiency Accentuates Vascular Inflammation and Atherosclerosis in the ApoE Knockout Mouse

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• Adenosine A1 Receptors Determine Glomerular Hyperfiltration and the Salt Paradox in Early Streptozotocin Diabetes Mellitus

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• Expression of ACE and ACE2 in individuals with diabetic kidney disease and healthy controls.

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• Decreased glomerular and tubular expression of ACE2 in patients with type 2 diabetes and kidney disease.

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• ACE2 Deficiency Modifies Renoprotection Afforded by ACE Inhibition in Experimental Diabetes

  2008influential reference
• ACE2 inhibition worsens glomerular injury in association with increased ACE expression in streptozotocin-induced diabetic mice.

  2007influential reference
• Diabetes‐induced hyperfiltration in adenosine A1‐receptor deficient mice lacking the tubuloglomerular feedback mechanism

  2007cited by this paper
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  2005cited by this paper
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  1987cited by this paper
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  1987cited by this paper
• Increased prostaglandin production by glomeruli isolated from rats with streptozotocin-induced diabetes mellitus.

  1985cited by this paper
• Activation of the tubuloglomerular feedback mechanism in dehydrated rats.

  1983cited by this paper
• Glomerular hemodynamics in experimental diabetes mellitus.

  1981influential reference
• Tubuloglomerular feedback and single nephron function after converting enzyme inhibition in the rat.

  1979cited by this paper

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  2018cites this paper
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  2018cites this paper
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