Células-tronco renais na hipertensão arterial sistêmica espontânea em ratos

Abstract

Systemic arterial hypertension (SAH) is a clinical condition that can lead to renal physiological changes. The kidneys have a concentration of renal mesenchymal stem cells (rMSCs) that can help repair kidney damage caused by hypertension. This study quantified the presence of rMSCs and RSCs (Renal stem cells) in rats with SAH (SHRs) at different stages of the disease: prehypertensive stage (4 weeks) and late hypertension stage (16 to 28 weeks), compared with normotensive rats (WKY). The CRSs were isolated from the kidneys of the animals in the different phases and subjected to flow cytometry for cell quantification of the c-Kit⁺CD45⁻ cells and showed that the different groups of young animals had similar numerical count in the SHR and WKY animals (0.55 ± 0.26% versus 0.25 ± 0.28% respectively, p = not significant). In adult animals, the numerical profile was significantly higher in SHRs compared to WKY rats of the same age (1.78 ± 0.31% versus 0.52 ± 0.24% in WKY rats, p <0.05). Regarding the quantification of rMSCs, counted as CFU-Fs (Fibroblast-like Colony Forming Units) per 10,000 cultured cells, the young SHR animals showed similar numerical count in their respective controls (6.6 ± 1.5 CFU-F / 10,000 cells versus 7.1 ± 1.6 CFU-F / 10,000 cells in the WKY group, respectively, p = NS). In adult animals, however, the CFU-Fs count was significantly higher in SHRs (58.1 ± 11.3 CFU-F / 10,000 cells in SHRs versus 21.2 ± 2.1 CFU-F / 10,000 cells in WKY rats, p <0.01). Microscopic renal morphometry revealed renal glomerular changes compatible with nephrosclerosis in adult SHRs in relation to the other groups, namely, the increase in the thickness of the Bowman's capsule (12.8 ± 0.6mm in adult SHRs versus 10.6 ± 0.8mm in adult WKY rats, p <0.05) and fibrosis. We conclude that the relationship between the increase in the amount of renal c-Kit⁺CD45⁻ mesenchymal stem cells and the increase in CFU-Fs in animals with SAH, suggests the possibility of their involvement in the pathophysiology of the disease.