【摘要】 已有心血管肥厚的SHR,给予卡托普利（Cap）20 mg·kg^-1·d^-1（A组）;可乐定（Clo）30μg·kg^-1·d^-1（B组）;Cap 20 mg·kg^-1·d^-1加 Clo 30 μg·kg^-1·d^-1（C组）;24周后处死,各组的SBP均明显下降,但未达WKY水平,Cap加Clo无更强降压作用,A组和C组的LVH明显逆转,两组间无差别,单用Clo不逆转SHR的LVH,各组的心肌NE明显降低,单用Cap的作用最强,说明Cap具有抗交感神经作用,且不因联用Clo而加强。更多还原

【Abstract】 Fifty-eight spontaneously hypertensive rats (SHR) at 12 wk of age were divided into 3 groups : A ) captopril ( Cap ) 2 0 mg· kg-1 · d-1 ; B ) clonidine ( Clo ) 3 0 μg · kg-1· d-1 ;C )Clo 30 μg ·kg-1 ·d-1 +Cap20mg ·kg-1·d-1 orally for 24 wk. Concomitant administration of Cap and Clo did not result in more lowering of the systolic blood pressure (SBP) than that by Cap alone. Regression of left ventricular hypertrophy (LVH) were remarkable in Groups A and C, but not to the extent in that of WKY. No significant difference between these two groups was found. Cap alone resulted in a greater decrease ofmyocardial norepinephrine ( NE) than that of Groups B and C. The wall/lumen ratio and the number of smooth muscle cell ( SMC) layers of renal artery decreased in Groups A andC, but little difference was found between them. It seemed that combined blockade of renin-angiotensin-aldosterone (RAA) system and sympathetic nervous system (SNS) did not produce more significant BP reduction and reversal of cardiovascular remodeling than Cap alone did. The sympathetic inhibitory effect of angiotensin converting enzyme inhibitor (ACEI) was not enhanced by sympatholytic treatment.更多还原