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  1. Article ; Online: Role of ADAMs in endothelial cell permeability: cadherin shedding and leukocyte rolling.

    Ponnuchamy, Bharathy / Khalil, Raouf A

    Circulation research

    2008  Volume 102, Issue 10, Page(s) 1139–1142

    MeSH term(s) ADAM Proteins/physiology ; Cadherins/physiology ; Capillary Permeability/physiology ; Endothelial Cells/cytology ; Endothelial Cells/physiology ; Humans ; Leukocyte Rolling/physiology ; Leukocytes/cytology ; Leukocytes/physiology
    Chemical Substances Cadherins ; ADAM Proteins (EC 3.4.24.-)
    Language English
    Publishing date 2008-05-22
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.108.177394
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article: Cellular mediators of renal vascular dysfunction in hypertension.

    Ponnuchamy, Bharathy / Khalil, Raouf A

    American journal of physiology. Regulatory, integrative and comparative physiology

    2009  Volume 296, Issue 4, Page(s) R1001–18

    Abstract: The renal vasculature plays a major role in the regulation of renal blood flow and the ability of the kidney to control the plasma volume and blood pressure. Renal vascular dysfunction is associated with renal vasoconstriction, decreased renal blood flow, ...

    Abstract The renal vasculature plays a major role in the regulation of renal blood flow and the ability of the kidney to control the plasma volume and blood pressure. Renal vascular dysfunction is associated with renal vasoconstriction, decreased renal blood flow, and consequent increase in plasma volume and has been demonstrated in several forms of hypertension (HTN), including genetic and salt-sensitive HTN. Several predisposing factors and cellular mediators have been implicated, but the relationship between their actions on the renal vasculature and the consequent effects on renal tubular function in the setting of HTN is not clearly defined. Gene mutations/defects in an ion channel, a membrane ion transporter, and/or a regulatory enzyme in the nephron and renal vasculature may be a primary cause of renal vascular dysfunction. Environmental risk factors, such as high dietary salt intake, vascular inflammation, and oxidative stress further promote renal vascular dysfunction. Renal endothelial cell dysfunction is manifested as a decrease in the release of vasodilatory mediators, such as nitric oxide, prostacyclin, and hyperpolarizing factors, and/or an increase in vasoconstrictive mediators, such as endothelin, angiotensin II, and thromboxane A(2). Also, an increase in the amount/activity of intracellular Ca(2+) concentration, protein kinase C, Rho kinase, and mitogen-activated protein kinase in vascular smooth muscle promotes renal vasoconstriction. Matrix metalloproteinases and their inhibitors could also modify the composition of the extracellular matrix and lead to renal vascular remodeling. Synergistic interactions between the genetic and environmental risk factors on the cellular mediators of renal vascular dysfunction cause persistent renal vasoconstriction, increased renal vascular resistance, and decreased renal blood flow, and, consequently, lead to a disturbance in the renal control mechanisms of water and electrolyte balance, increased plasma volume, and HTN. Targeting the underlying genetic defects, environmental risk factors, and the aberrant renal vascular mediators involved should provide complementary strategies in the management of HTN.
    MeSH term(s) Animals ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Extracellular Matrix/metabolism ; Genetic Predisposition to Disease ; Humans ; Hypertension/complications ; Hypertension/metabolism ; Hypertension/physiopathology ; Kidney/blood supply ; Kidney Diseases/etiology ; Kidney Diseases/metabolism ; Kidney Diseases/physiopathology ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/physiopathology ; Oxidative Stress ; Renal Circulation ; Risk Factors ; Signal Transduction ; Sodium Chloride, Dietary/adverse effects ; Vasculitis/complications
    Chemical Substances Sodium Chloride, Dietary
    Language English
    Publishing date 2009-02-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.90960.2008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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