Angiotensin involvement in kidney injury induced by rheumatoid arthritis in rat

Author(s):Show less -

Carlos, Carla Patricia ^[1] ; de Carvalho, Enzo Prandi ^[1] ; Angeli Junior, Euradir Vitorio ^[1] ; Garcia Filho, Glayber Falcao ^[1] ; Dona, Joao Pedro Lot ^[1] ; Batanero, Rodrigo Piloto de Oliveira ^[1] ; Guena, Rafael de Oliveira ^[1] ; Agren, Camila ^[1] ; Baptista, Maria Alice Sperto Ferreira ^[2] ; Bizotto, Thais Santana Gastardelo ^[3] ; Cury, Patricia Maluf ^[1] ; Chies, Agnaldo Bruno ^[4]

Affiliation

^[1] FACERES Sch Med, Lab Expt Res, Sao Jose Do Rio Preto, SP - Brazil

^[2] FUNFARME FAMERP Sch Med, Dept Nephrol & Pathol, Sao Jose Do Rio Preto, SP - Brazil

^[3] FUNFARME FAMERP Sch Med, Dept Mol Biol, Sao Jose Do Rio Preto, SP - Brazil

^[4] FAMEMA, Lab Pharmacol, Marilia Med Sch, Sao Paulo, Marilia - Brazil

• Document type: Journal article
• Source: Clinical and Experimental Pharmacology and Physiology; v. 48, n. 9, p. 1271-1279, SEP 2021.
• Web of Science Citations: 0

Abstract

Renal injury induced by rheumatoid arthritis is not clear and may be related to the angiotensin II. We aim to investigate the adjuvant-induced arthritis (AIA) injury in rat kidney, focusing the angiotensin II/AT(1) pathway. Male Wistar rats were allocated in to three groups: Control, AIA and AIA plus losartan. The AIA was induced by injection of 100 mu L of an emulsion of dissected Mycobacterium tuberculosis (50 mg/mL) on the paw. Treatment with losartan was initiated on the first day of immunization (daily subcutaneous injection, 1 mg/kg). After 60 days post immunization, we evaluated kidney function by plasma creatinine, urea and uric acid levels and creatinine depuration; kidney injury by apoptosis analysis and inflammation markers such as macrophages, transforming growth factor beta (TGF-beta) and inducible nitric oxide synthase (iNOS) expression; oxidative stress by plasma thiobarbituric acid reactive substances (TBARS); renal expression of angiotensin receptors subtype 1 (AT(1)) and 2 (AT(2)) and plasma concentration of angiotensin II. AIA rats showed elevated plasma levels of creatinine, urea, uric acid, TBARS and Ang II and reduced creatinine depuration, and enhanced kidney macrophage number, TGF-beta, caspase-3, iNOS and AT(1)/AT(2) receptors expression. The losartan reduced plasma creatinine and its clearance, reduced macrophages and the expression of TGF-beta and iNOS in renal tissues, and reduced plasma TBARS. We conclude that AIA causes kidney injury by a physiopathological mechanism that involves AT(1) stimulation in renal tissue, elevating the presence of macrophages, the expression of TGF-beta and iNOS, as well the local oxidative stress, which contribute to renal function deterioration. (AU)

• FAPESP's process: 16/08450-3 - Influence of testosterone in the vascular changes promoted by adjuvant-induced arthritis that involves angiotensin II
• Grantee: Agnaldo Bruno Chies
• Support Opportunities: Regular Research Grants
• FAPESP's process: 17/18730-6 - Evaluation of renal function and plasma level of TBARS in arthritic rats
• Grantee: Rodrigo Piloto de Oliveira Batanero
• Support Opportunities: Scholarships in Brazil - Scientific Initiation