中皮質ネフロン
WordNet
- any of the small tubules that are the excretory units of the vertebrate kidney (同)uriniferous_tubule
UpToDate Contents
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
English Journal
- Bimoclomol ameliorates mercuric chloride nephrotoxicity through recruitment of stress proteins.
- Stacchiotti A1, Borsani E, Ricci F, Lavazza A, Rezzani R, Bianchi R, Rodella LF.Author information 1Division of Human Anatomy, Department of Biomedical Sciences and Biotechnology, University of Brescia, Viale Europa 11, I 25123 Brescia, Italy. stacchio@med.unibs.itAbstractBimoclomol (BIM), is a stress proteins coinducer, that acts synergistically with a mild stressor to activate cytoprotective stress proteins. BIM has been successfully utilized in animal models for the treatment of various nervous, cardiac and cerebrovascular diseases. Mercuric chloride (HgCl(2)) induces acute renal failure in rats by a single dosage. The present in vivo study was conducted to assess the efficacy of BIM against acute HgCl(2) nephrotoxicity. At different times after BIM and/or HgCl(2) exposure we evaluated renal morphology and the localization/abundance of three stress proteins (HSP72, GRP75, HSP60) by electron microscopy, immunohistochemistry and Western blot analysis. BIM delivery to rats 6h before mercury, ameliorated damage to renal ultrastructure, with recovery of tubular and mitochondrial membranes 24h after mercury treatment. In rats pretreated with BIM prior to HgCl(2) exposure, HSP72 was significantly overexpressed in proximal tubules in a time-dependent manner. In contrast, the amounts of GRP75 and HSP60 after BIM pretreatment were comparable to the group treated with mercury alone, but these stress proteins had translocated to the nuclei at 14 and 24h, respectively. These novel findings suggest that BIM mitigates HgCl(2) nephrotoxicity in rats through the early recruitment of stress proteins in midcortical proximal tubules that are the main renal mercury-targets.
- Toxicology letters.Toxicol Lett.2006 Oct 10;166(2):168-77. Epub 2006 Jun 30.
- Bimoclomol (BIM), is a stress proteins coinducer, that acts synergistically with a mild stressor to activate cytoprotective stress proteins. BIM has been successfully utilized in animal models for the treatment of various nervous, cardiac and cerebrovascular diseases. Mercuric chloride (HgCl(2)) ind
- PMID 16891066
- Stress proteins expression in rat kidney and liver chronically exposed to aluminium sulphate.
- Stacchiotti A1, Rodella LF, Ricci F, Rezzani R, Lavazza A, Bianchi R.Author information 1Division of Human Anatomy, Department of Biomedical Sciences and Biotechnology, University of Brescia, Brescia, Italy. stacchio@med.unibs.itAbstractAluminium (Al) is the third most widespread metal in the environment. It is toxic for the brain, bone and haematological system but unfortunately very little data exist for other organs. Stress proteins are induced or enhanced against metal toxicity with an essential role in the recovery of organules and other cellular proteins. This immunohistochemical study was performed to analyze the distribution of three stress proteins (HSP25, HSP72, GRP75) in rat kidney and liver orally exposed to Al sulphate daily for 3 and 6 months. Al-induced alterations were further studied by histopathology (H-E, PAS, Perl's, Masson) and ultrastructural morphometry. In the kidney: HSP25 was enhanced in proximal tubules after 6 months Al-exposure when abnormal brush borders were observed; HSP72 was induced in proximal tubules only after long Al-treatment; GRP75 was raised in midcortical area sometimes within nuclei. Furthermore, lysosomal and lipofuscins densities increased in the juxtamedullary tubules after 3 months Al exposure with respect to controls. In the liver: Perl's-positive deposits and fibrosis became evident after Al treatment. HSP25 was very weak; HSP72 focal in pericentral hepatocytes at 3 months and induced also in Kupffer cells at 6 months; GRP75 diffuse in periportal hepatocytes and non parenchymal cells at 6 months. Prolonged Al exposure stimulated stress proteins strictly organ-dependently in the rat. Their distribution in kidney and liver seems related to cumulative sublethal effects induced by metal and could be a sensitive index of Al susceptibility of these organs.
- Histology and histopathology.Histol Histopathol.2006 Feb;21(2):131-40.
- Aluminium (Al) is the third most widespread metal in the environment. It is toxic for the brain, bone and haematological system but unfortunately very little data exist for other organs. Stress proteins are induced or enhanced against metal toxicity with an essential role in the recovery of organule
- PMID 16329037
- Vasoconstrictor and vasodilator effects of adenosine in the kidney.
- Hansen PB1, Schnermann J.Author information 1National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.AbstractAdenosine is an ATP breakdown product that in most vessels causes vasodilatation and that contributes to the metabolic control of organ perfusion, i.e., to the match between oxygen demand and oxygen delivery. In the renal vasculature, in contrast, adenosine can produce vasoconstriction, a response that has been suggested to be an organ-specific version of metabolic control designed to restrict organ perfusion when transport work increases. However, the vasoconstriction elicited by an intravenous infusion of adenosine is only short lasting, being replaced within 1-2 min by vasodilatation. It appears that the steady-state response to the increase of plasma adenosine levels above normal resulting from the infusion is global renal vasorelaxation that is the result of A2AR activation in most parts of the renal vasculature, including larger renal arteries, juxtamedullary afferent arterioles, efferent arterioles, and medullary vessels. A2AR-mediated vasorelaxation is probably facilitated by endothelial receptors that cause the release of nitric oxide and other endothelial relaxing factors. In contrast, isolated perfused afferent arterioles of superficial and midcortical nephrons of rabbit and mouse, especially in their most distal segment at the entrance to the glomerulus, respond to adenosine with persistent vasoconstriction, indicating predominant or exclusive expression of A1AR. A1AR in afferent arterioles are selectively activated from the interstitial aspect of the vessel. This property can dissociate A1AR activation from changes in vascular adenosine concentration, a characteristic that is ideally suited for the role of renal adenosine as a paracrine factor in the control of glomerular function.
- American journal of physiology. Renal physiology.Am J Physiol Renal Physiol.2003 Oct;285(4):F590-9.
- Adenosine is an ATP breakdown product that in most vessels causes vasodilatation and that contributes to the metabolic control of organ perfusion, i.e., to the match between oxygen demand and oxygen delivery. In the renal vasculature, in contrast, adenosine can produce vasoconstriction, a response t
- PMID 12954591
Related Links
- Looking for online definition of Cortical nephron in the Medical Dictionary? Cortical nephron explanation free. What is Cortical nephron? Meaning of Cortical nephron medical term. What does Cortical nephron mean? http://medical ...
- a. glomerular region (renal corpuscle; about 0.2 mm diameter) 1) glomerulus (capillary tuft) 2) Bowman's capsule (blind end of the nephron) (note: Bowman's capsule and the glomerulus together are named the Malpigian ...
★リンクテーブル★
[★]
- 英
- midcortical nephron
- 関
- 短ループネフロン