Introduction: Tribulus terrestris is a plant that increases serum testosterone levels when ingested and has been widely used by people seeking an increase in muscle mass and libido. Testosterone supplementation may increase the risk of hypertension and risk of acute and chronic renal failure. Rats of the spontaneously hypertensive lineage (SHR) have an increase in blood pressure, being an ideal animal model for this study. The objective of this study is to quantitatively evaluate renal cortex of normotensive and hypertensive rats after treatment with Tribulus terrestris.
Methods: We used 28 rats divided into 4 groups: N - group composed of untreated Wistar Kyoto (normotensive) rats; NT -Kyoto Wistar rats treated with Tribulus terrestris (100mg/Kg/day); H - untreated SHR; HT - SHR treated with Tribulus terrestris (100mg/Kg/day). The drug was administered by gavage for 40 days. The initial mean arterial pressure (iMAP) and final mean arterial pressure (fMAP) were measured by tail plethysmography. The day after the end of treatment, the kidneys were collected and processed for histomorphometric analysis. The renal volume, the cortex/non-cortex ratio, the glomerular volumetric density (Vv[Glom]), the weighted mean glomerular volume (VWGV) and number of glomeruli per kidney (N[Glom]) were evaluated and compared by one-way ANOVA with Bonferroni post-test. Student’s paired T test was used for comparison of iMAP and fMAP. All results were considered significant when the value of p<0.05.
Results: The fMAP was 57.4% higher than the iMAP in the NT group. The renal volume and the cortex/non-cortex ratio did not present significant differences between groups. The Vv[Glom] of the NT group was decreased in 29% when compared to the N group, as also did the HT group in relation with H group in 39.7%. VWGV of group NT was lower when compared with N group in 27.1%. The N[Glom] of group HT was 48.5% lower when compared to the group H.
Conclusions: The supplementation with Tribulus terrestris promotes considerable damage to the kidney of normotensive and hypertensive rats. Source of
Funding: Supported by grants from CNPq, FAPERJ and CAPES.