INTERACTION BETWEEN ANGIOTENSIN II, HYPERTENSION AND INFLAMMATION IN RAT KIDNEY

The renin-angiotensin system is one of the most important regulatory mechanisms of blood pressure homeostasis. Hypertension, a risk factor for chronic kidney disease, is able to induce renal injury by promoting inflammation. Inflammatory cytokines can induce fibrosis in various organs, including the kidney. Aim: The study verifies if angiotensin II is implicated in kidney T cells infiltration. Material and Methods: The experiment was performed on Wistar male rats, divided in two groups who received either a sham operation (control group, n = 9) or continuous angiotensin II (Ang II) infusion (300ng/kgc/min)(Ang II group, n = 9) subcutaneously, via minipumps. Blood pressure was measured noninvasively (tail cuff). After 14 days, the animals were sacrificed under anesthesia with xylazine/ketamine. The tissue obtained of each kidney was used for histopathological exam or flow cytometry. Renal inflammation was assessed using a flow cytometric analysis. The Histo Quest program quantified automatically the cellular elements and performed a statistical analysis on the obtained data. Results: Inflammation was observed in Ang II Wistar rats group, accompanied by an increase in renal CD45RC+, CD45RA+, CD19+. Conclusions: Our research underlines an undefined role for T cells in the genesis of high blood pressure up to that time and sustains the involvement of inflammation in the pathogenesis of this prevalent disease. Thus, T cells might correspond to a novel therapeutic target for the management of hypertension.