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Renal expression of angiotensin type 2 (AT2) receptors during kidney damage

2003; Elsevier BV; Volume: 64; Linguagem: Inglês

10.1046/j.1523-1755.64.s86.5.x

1523-1755

Marta Ruíz-Ortega, Vanesa Esteban, Yusuke Suzuki, Mónica Rupérez, Sergio Mezzano, Leopoldo Ardiles, Pilar Justo, Alberto Ortíz, Jesús Egido,

Hormonal Regulation and Hypertension

Renal expression of angiotensin type 2 (AT2) receptors during kidney damage. Background Activation of the renin angiotensin system has been described in pathologic conditions, including kidney damage. Angiotensin II (Ang II) acts through two receptors, AT 1 and AT 2 . Most of the known actions of Ang II, including vasoconstriction and fibrosis, are due to AT 1 activation. Recent data suggest that AT 2 participates in the regulation of cell growth and renal inflammatory infiltration. Therefore, we investigated the renal expression of AT 2 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. AT 2 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 AT 2 were found. Ang II infusion resulted in an up-regulation of AT 2 in tubular cells and de novo AT 2 expression in glomeruli and vessels, associated with the presence of inflammatory cells. Acute tubular injury induced by folic acid was characterized by AT 2 overexpression and apoptosis in tubular cells. Protein overload caused heavy proteinuria and tubular AT 2 up-regulation. Conclusion AT 2 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.