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      Autoregulation of Total and Zonal Glomerular Filtration Rate in Spontaneously Hypertensive Rats with Mesangiolysis

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          Abstract

          In this study we tested the hypothesis that mesangial cells participate in autoregulation of the glomerular filtration rate (GFR) in normotensive and hypertensive rats. Mesangial cell lesions were induced by intravenous administration of antithymocyte (anti-Thy 1.1) antibodies in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto rats (WKY). Normal murine serum was injected in control rats. Hemodynamic measurements were performed 24 h after the infusion of the anti-Thy 1.1 antibodies. Renal blood flow (RBF) was measured by a transit time flowmeter (Transonic) and the GFR was measured as the uptake of <sup>125</sup> iodine-labeled aprotinin (<sup>125</sup>I-Ap) by proximal tubular cells at the control renal arterial pressure and <sup>131</sup>I-Ap at a pressure reduction close to the lower pressure limit of RBF autoregulation. RBF was unaltered and the autoregulatory capability was maintained in SHR and WKY after mesangial cell lesions. Mesangiolysis significantly reduced the total GFR in normotensive, but not in hypertensive animals. The fractional compensation of the GFR was attenuated in the outer cortical layer (p < 0.05) in normotensive WKY In SHRs the fractional compensation of the GFR was impaired in all cortical layers after mesangiolysis, slightly more in the outer than in the inner cortex. We conclude that mesangial cells may contribute to the autoregulation of GFR in hypertensive rats, but to a lesser extent in normotensive rats.

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          Author and article information

          Journal
          KBR
          Kidney Blood Press Res
          10.1159/issn.1420-4096
          Kidney and Blood Pressure Research
          S. Karger AG
          1420-4096
          1423-0143
          1997
          1997
          11 November 2008
          : 20
          : 1
          : 11-17
          Affiliations
          aRenal Research Group, Medical Department A, Haukeland Hospital, and Departments of bPhysiology and cPathology, University of Bergen, Norway
          Article
          174105 Kidney Blood Press Res 1997;20:11–17
          10.1159/000174105
          9192905
          © 1997 S. Karger AG, Basel

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          Page count
          Pages: 7
          Categories
          Original Paper

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