Volume 8 | Issue - 8
Volume 8 | Issue - 8
Volume 8 | Issue - 8
Volume 8 | Issue - 7
Volume 8 | Issue - 7
Introduction: The renin-angiotensin-aldosterone system (RAAS) plays a central role in regulating renal hemodynamics, particularly through angiotensin II, which contributes to hypertension-induced nephron damage. While ACE inhibitors are well-established for their hemodynamic benefits in hypertension and chronic kidney disease, their impact on nephron microanatomy remains underexplored. This study evaluates the structural and functional renal effects of chronic ACE inhibition using Enalapril in a hypertensive rat model. Materials and Methods: An experimental, randomized, controlled study was conducted using 30 male Wistar rats divided into three groups (n = 10 each): • Group I (Control): received normal saline. • Group II (Hypertensive): hypertension induced with L-NAME (40 mg/kg/day) for 2 weeks. • Group III (ACEI-Treated): hypertensive rats treated with Enalapril (10 mg/kg/day) for 8 weeks. Parameters assessed included systolic blood pressure (tail-cuff method), serum creatinine, blood urea nitrogen (BUN), and histological evaluation of glomerular sclerosis, tubular epithelial thickness, and interstitial fibrosis. Statistical analysis was done using one-way ANOVA followed by Tukey’s post hoc test (p < 0.05 considered significant). Results: Hypertensive rats showed significantly elevated blood pressure, serum creatinine, BUN, and marked nephron damage (glomerular sclerosis score 3.2 ± 0.5). ACEI treatment reduced systolic BP (130.3 ± 6.2 mmHg), improved serum creatinine (0.72 ± 0.08 mg/dL), and decreased glomerular sclerosis (1.2 ± 0.6). Histological improvements included reduced tubular thickening and interstitial fibrosis. Significant correlations were observed between functional parameters and histological changes (e.g., serum creatinine vs. glomerular sclerosis: r = 0.82, p < 0.001). Conclusion: Chronic administration of Enalapril provides significant protection against hypertensive renal injury by reducing both functional impairment and histological damage. These findings highlight the structural benefits of ACE inhibitors in nephron preservation and emphasize the importance of combining pharmacological and anatomical assessments i