| Objective:To observe the pathologic changes and endothelin-1 (ET-1) expression in kidney after aldosterone infusion and to explore the mechanisms of persistence of hypertension in primary aldosteronism (PA) patients after operation.Methods:SD (Sprague-Dawley) rats were randomly divided into 3 groups, with each group 8 rats. Aldosterone group: aldosterone infusion (1μg/h) via a mini-osmotic pump implanted subcutaneously; Aldosterone plus spironolactone group: equal doses of aldosterone infusion and gastric gavage with spironolactone (100mg·kg-1·d-1); Control group: only vehicle infusion. Systolic blood pressure (SBP) was monitored by the tail-cuff method. The concentration of sodium, potassium and aldosterone in blood serum and plasma rennin activity (PRA) were measured after 4 weeks. Observing the changes of histomorphology and fibrosis in kidney via HE and Masson dying, respectively. RT-PCR and immunohistochemistry for detecting the expression and localization of ET-1 in renal tissue, respectively.Results:Aldosterone significantly elevated SBP after 2 weeks and decreased the concentration of potassium, presenting the characteristic of low- rennin and high-aldosterone compared to control group (P<0.01). Aldosterone promoted renal fibrosis and significantly up-regulated the expression of ET-1 compared to control group (P<0.01), spironolactone could inhibite the effect above (P<0.01).Conclusions:Aldosterone may promote renal fibrosis via up-regulating the expression of ET-1 gene in renal tubular epithelial cells, and then leads to irreversible renal leisions and renal hypertension subsequently, which may be one of the mechanisms of persistence of hypertension in PA patients after operation. |
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