EFFECTS OF SPIRONOLACTONE ON LEFT VENTRICULAR HYPERTROPHY AND PLASMA ADRENOMEDULLIN CONCENTRATION IN HYPERTENSIVE RATS
Xing Yu
Abstract
Xing Yu
Abstract
ObjectiveTo investigate the effects of spironolactone on cardiac structure and function, and the concentration of plasma adrenomedullin in hypetrensive rats. MethodsThe model of hypertensive rat was established by abdominal aortic constriction. Fouty-four male Wistar rats were randomly divided into four groups: hypertension group (hypertensive rats serving as controls), derindopril group (hypertensive rats subjected to derindopril treatment, (2 mg/(kg·d)), spironolactone group (hypertensive rats receiving spironolactone treatment,(20 mg/(kg·d),) control group (sham operated rats serving as controls), each group has 11 rats. After treatment of 12 weeks, cardiac structure and function were detected in all groups by ultrosonography, and then plasma adrenomedullin were examined by radioimmunity. ResultsCompared with hypertension group, interventricular septal thickness (IVSTd), left ventricular posterior wall thickness (LVPWTd), relative wall thickness(RWT) of left vertricular, left ventricular mass (LVM), left ventricular end-diastolic diameter (LVEDD), left atrial diameter (LAD) in spironolactone group and derindopril group decreased significantly (P(0.01), P(0.05)). Spironolactone group decreased more than derindopril group in RWT(P(0.01)). Compared with hypertension group both spironolactone and derindopril attenuated the increases of plasma ADM (P(0.01)). ConclusionBoth spironolactone and derindopril attenuate the increase of left ventricular hypertrophy and improve left ventricular diastolic function. Spironlactone is much more effective than derindopril in preventing left ventricular hypertrophy. After treament of spironolactone and derindopril plasma ADM decreased, companying the improvement of left ventricular hypertrophy and diastolic function, the mechanism may be that plasma ADM played a compensatory role through inhibition renin angiotensin aldosterone system and (or) a direct effect.
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ObjectiveTo investigate the effects of spironolactone on cardiac structure and function, and the concentration of plasma adrenomedullin in hypetrensive rats. MethodsThe model of hypertensive rat was established by abdominal aortic constriction. Fouty-four male Wistar rats were randomly divided into four groups: hypertension group (hypertensive rats serving as controls), derindopril group (hypertensive rats subjected to derindopril treatment, (2 mg/(kg·d)), spironolactone group (hypertensive rats receiving spironolactone treatment,(20 mg/(kg·d),) control group (sham operated rats serving as controls), each group has 11 rats. After treatment of 12 weeks, cardiac structure and function were detected in all groups by ultrosonography, and then plasma adrenomedullin were examined by radioimmunity. ResultsCompared with hypertension group, interventricular septal thickness (IVSTd), left ventricular posterior wall thickness (LVPWTd), relative wall thickness(RWT) of left vertricular, left ventricular mass (LVM), left ventricular end-diastolic diameter (LVEDD), left atrial diameter (LAD) in spironolactone group and derindopril group decreased significantly (P(0.01), P(0.05)). Spironolactone group decreased more than derindopril group in RWT(P(0.01)). Compared with hypertension group both spironolactone and derindopril attenuated the increases of plasma ADM (P(0.01)). ConclusionBoth spironolactone and derindopril attenuate the increase of left ventricular hypertrophy and improve left ventricular diastolic function. Spironlactone is much more effective than derindopril in preventing left ventricular hypertrophy. After treament of spironolactone and derindopril plasma ADM decreased, companying the improvement of left ventricular hypertrophy and diastolic function, the mechanism may be that plasma ADM played a compensatory role through inhibition renin angiotensin aldosterone system and (or) a direct effect.
Key concepts: Spironolactone, Adrenomedullin, Internal medicine, Medicine, Left ventricular hypertrophy, Aldosterone, Muscle hypertrophy, Endocrinology