Abstract

INTRODUCTION AND OBJECTIVES: The target organ damage is well documented in arterial hypertension, but testicular damage is not clearly defined. This study evaluates the testicular morphology and spermatozoid parameters of spontaneously hypertensive rats (SHR) treated or not with enalapril. METHODS: 28 adult SHR animals were assigned into two groups, a hypertensive group (H, n 13), and an enalapril treated group (HE, n 15). Wistar-Kyoto rats (WKY, n 8) were used as controls. Animals of group HE received 30mg/Kg of enalapril daily by gavage while H and WKY animals received tap water. Arterial systolic pressure was weekly measured by plethysmography. After five weeks of treatment, all animals were killed by anesthetic overdose. The right epididimal tail was removed and used for spermatozoid collection. Sperm concentration, motility and viability (hypo-osmotic test) were assessed. The right testicles were fixed and routinely processed for obtaining hematoxylin and eosin stained histological sections. In these sections, the seminiferous tubule diameter, epithelial height and relative densities of the testicular structures were assessed by stereological methods. All data was compared by ANOVA with Tukey’s post test, considering p 0.05 as significant. RESULTS: Blood pressure in the HE group were similar WKY, and lower than H animals. Spermatozoid concentration had a 38% reduction in hypertensive rats when compared to controls while enalapril treatment restored normal concentration. Concerning spermatozoid motility and viability, no difference was found among the groups. Testicular vascular volumetric density was also altered in hypertensive group while HE animals were similar to controls. The seminiferous epithelium of HE animals showed the highest volumetric density, indicating a positive effect of enalapril in spermatogenesis. The analysis of seminiferous tubule diameter and epithelium height showed no significant difference among the studied groups. Table 1 presents all numerical data. CONCLUSIONS: In the SHR model, hypertension induces testicular alterations both in seminiferous tubule and intratesticular vessels resulting in low spermatozoid concentration. Enalapril treatement partially protected the testicle from the hypertension-induced alterations, restoring normal spermatozoid production. Source of Funding: FAPERJ, CNPq and CAPES.

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