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Research Article

Pro-inflammatory role of angiotensin II in mercuric chloride-induced nephropathy in rats

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Pages 125-132 | Received 12 Apr 2012, Accepted 28 May 2012, Published online: 23 Jul 2012

Figures & data

Figure 1.  Renal interstitial expression of angiotensin II (AngII), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and macrophages (ED-1) in HgCl2-induced nephropathy. Increased expressions of (a) Ang II, (b) ICAM-1, (c) ED-1 (macrophages), and (d) iNOS were observed in all HgCl2-treated rats. Losartan and Enalapril diminished the induced expression of those molecules. Values shown are mean (± SD) from 10 rats/group.

Figure 1.  Renal interstitial expression of angiotensin II (AngII), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and macrophages (ED-1) in HgCl2-induced nephropathy. Increased expressions of (a) Ang II, (b) ICAM-1, (c) ED-1 (macrophages), and (d) iNOS were observed in all HgCl2-treated rats. Losartan and Enalapril diminished the induced expression of those molecules. Values shown are mean (± SD) from 10 rats/group.

Figure 2.  Renal tubular expressions of angiotensin II (AngII), intercellular adhesion molecule-1 (ICAM-1), and inducible nitric oxide synthase (iNOS) in HgCl2-induced nephropathy. Increased expressions of (a) Ang II, (b) ICAM-1, and (c) iNOS were observed in all HgCl2-treated rats. Enalapril diminished the expression of AngII and both Enalapril and Losartan diminished the expressions of ICAM-1 and INOS.

Figure 2.  Renal tubular expressions of angiotensin II (AngII), intercellular adhesion molecule-1 (ICAM-1), and inducible nitric oxide synthase (iNOS) in HgCl2-induced nephropathy. Increased expressions of (a) Ang II, (b) ICAM-1, and (c) iNOS were observed in all HgCl2-treated rats. Enalapril diminished the expression of AngII and both Enalapril and Losartan diminished the expressions of ICAM-1 and INOS.

Figure 3.  Immunofluorescence of renal angiotensin II (AngII), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and macrophages (ED-1) in HgCl2-induced nephropathy. (a) Intense tubular expression of Ang II in tubules (arrows) and in interstitial cells (arrowheads). Magnification: ×100. (b) ICAM-1 expression in brush border of proximal tubules (arrows) and in interstitial cells (arrowheads). Magnification: ×400. (c) Increased infiltration of ED-1+ cells in tubulo-interstitial areas (arrows). Magnification: ×400. (d) iNOS+ cells in tubulo-interstitial areas (arrows). Magnification: ×400.

Figure 3.  Immunofluorescence of renal angiotensin II (AngII), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and macrophages (ED-1) in HgCl2-induced nephropathy. (a) Intense tubular expression of Ang II in tubules (arrows) and in interstitial cells (arrowheads). Magnification: ×100. (b) ICAM-1 expression in brush border of proximal tubules (arrows) and in interstitial cells (arrowheads). Magnification: ×400. (c) Increased infiltration of ED-1+ cells in tubulo-interstitial areas (arrows). Magnification: ×400. (d) iNOS+ cells in tubulo-interstitial areas (arrows). Magnification: ×400.

Figure 4.  Glomerular expression of angiotensin II (AngII), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and macrophages (ED-1) in HgCl2-induced nephropathy. In general, expression of (a) Ang II and the (b, c, d) pro-inflammatory molecules remained similar to control values. Values shown are mean (± SD) from 10 rats/group.

Figure 4.  Glomerular expression of angiotensin II (AngII), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and macrophages (ED-1) in HgCl2-induced nephropathy. In general, expression of (a) Ang II and the (b, c, d) pro-inflammatory molecules remained similar to control values. Values shown are mean (± SD) from 10 rats/group.

Table 1.  Proximal tubule changes in HgCl2 nephropathy.

Table 2.  Serum creatinine and renal protein excretion in HgCl2 nephropathy.

Table 3.  Interstitial and tubular correlations of angiotensin II, ICAM-1, iNOS, and infiltration of ED-1+ cells.

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