Abstract: Objective:The present study was designed to detect anti-fibrotic effects of low dose aldosterone（ALDO） receptor anatagonist-spironolactone （spiron） on the sustained hypertensive myocardial fibrosis induced by LNNA. Methods:The plasma and myocardial angiotensin Ⅱ（AⅡ） and ALDO, serum NO₂^- and left ventrical myocardial collagen content （C） were determined in the untreated and treated 18 rat models of hypertensive myocardial fibrosis with spiron （20 mg/kg,1/d, by gavage）and in control （7 wistar rats）. Results:（1）The natural regressive effects were found in serum NO₂^-（P＜0.05） and arterial blood pressure （ABP） （P＜0.01）. But the natural regression in heart-body weight ratio （HWR） and C weren't found. （2）The spiron treatment abolished the significant increases in the levels of HWR, AⅡ, but didn't affact ABP and the level of serum NO₂^-.Conclusion:These data suggest that the development of myocardial fibrosis in this model may be related to the increase in the density of ALDO binding with its receptors mediated by the decrease of NO synthesis, and the low dose spiron treatment may make the myocardial fibrosis regress, possibly via its competitive inhibiting action at ALDO binding with its receptors.