BACKGROUND: Activation of the renin angiotensin system has been described in pathologic conditions, including kidney damage. Angiotensin II (Ang II) acts through two receptors, AT1 and AT2. Most of the known actions of Ang II, including vasoconstriction and fibrosis, are due to AT1 activation. Recent data suggest that AT2 participates in the regulation of cell growth and renal inflammatory infiltration. Therefore, we investigated the renal expression of AT2 receptors in several models of renal injury. METHODS: Investigations were done in the following experimental models of kidney damage: systemic infusion of Ang II (inflammation), folic acid nephropathy (tubular cell death), and protein overload proteinuria. AT2 expression was determined by immunohistochemistry (protein) and reverse transcription-polymerase chain reaction (RT-PCR) (gene). RESULTS: In control animals, low levels of renal expression of AT2 were found. Ang II infusion resulted in an up-regulation of AT2 in tubular cells and de novo AT2 expression in glomeruli and vessels, associated with the presence of inflammatory cells. Acute tubular injury induced by folic acid was characterized by AT2 overexpression and apoptosis in tubular cells. Protein overload caused heavy proteinuria and tubular AT2 up-regulation. CONCLUSION: AT2 is re-expressed in pathologic conditions of kidney damage, such as inflammation, apoptosis, and proteinuria, suggesting a potential role of this receptor during renal injury.
BACKGROUND: Activation of the renin angiotensin system has been described in pathologic conditions, including kidney damage. Angiotensin II (Ang II) acts through two receptors, AT1 and AT2. Most of the known actions of Ang II, including vasoconstriction and fibrosis, are due to AT1 activation. Recent data suggest that AT2 participates in the regulation of cell growth and renal inflammatory infiltration. Therefore, we investigated the renal expression of AT2 receptors in several models of renal injury. METHODS: Investigations were done in the following experimental models of kidney damage: systemic infusion of Ang II (inflammation), folic acidnephropathy (tubular cell death), and protein overload proteinuria. AT2 expression was determined by immunohistochemistry (protein) and reverse transcription-polymerase chain reaction (RT-PCR) (gene). RESULTS: In control animals, low levels of renal expression of AT2 were found. Ang II infusion resulted in an up-regulation of AT2 in tubular cells and de novo AT2 expression in glomeruli and vessels, associated with the presence of inflammatory cells. Acute tubular injury induced by folic acid was characterized by AT2 overexpression and apoptosis in tubular cells. Protein overload caused heavy proteinuria and tubular AT2 up-regulation. CONCLUSION:AT2 is re-expressed in pathologic conditions of kidney damage, such as inflammation, apoptosis, and proteinuria, suggesting a potential role of this receptor during renal injury.
Authors: Bruno Sevá Pessôa; Nils van der Lubbe; Koen Verdonk; Anton J M Roks; Ewout J Hoorn; A H Jan Danser Journal: Nat Rev Nephrol Date: 2012-11-20 Impact factor: 28.314
Authors: Nyssa E Hoch; Tomasz J Guzik; Wei Chen; Tenecia Deans; Samer A Maalouf; Petra Gratze; Cornelia Weyand; David G Harrison Journal: Am J Physiol Regul Integr Comp Physiol Date: 2008-12-10 Impact factor: 3.619
Authors: A Koïtka; Z Cao; P Koh; A M D Watson; K C Sourris; L Loufrani; A Soro-Paavonen; T Walther; K J Woollard; K A M Jandeleit-Dahm; M E Cooper; T J Allen Journal: Diabetologia Date: 2009-12-03 Impact factor: 10.122