Liang Y H, Wang J M, Zhou Y, Jiang X J, Jiang H, Huang C X
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan city, Hubei province, 430060, PR China.
Life Sci. 2004 Aug 27;75(15):1871-8. doi: 10.1016/j.lfs.2004.04.012.
The additive effects of combined valsartan and spironolactone on plasma and cardiac aldosterone escape were evaluated in spontaneously hypertensive rats (SHRs). Twenty-four SHRs were treated with valsartan (30 mg/kg body weight per day), spironolactone (20 mg/kg body weight per day) and a combination of both for 4 months. Blood was collected and plasma aldosterone (PA) was estimated with radioimmunoassay (RIA). Ex vivo heart perfusion was performed, the ex vivo cardiac aldosterone (EXCA) was assessed by RIA after high-performance liquid chromatography separation. PA and EXCA were significantly decreased after one month but increased after 4 months in valsartan administration group. The combined valsartan and spironolactone therapy normalized cardiac aldosterone levels. This study provides the first evidence that the long-term treatment with Angiotensin II type 1 receptor antagonist (AT1A) induces local aldosterone escape in cardiovascular tissue, whereas the combined AT1A and spironolactone therapy inhibits the escape in hypertensive rats.
在自发性高血压大鼠(SHR)中评估缬沙坦和螺内酯联合使用对血浆和心脏醛固酮逃逸的附加作用。24只SHR分别接受缬沙坦(每天30mg/kg体重)、螺内酯(每天20mg/kg体重)以及两者联合治疗4个月。采集血液,用放射免疫分析法(RIA)测定血浆醛固酮(PA)。进行离体心脏灌注,高效液相色谱分离后用RIA评估离体心脏醛固酮(EXCA)。缬沙坦给药组中,PA和EXCA在1个月后显著降低,但在4个月后升高。缬沙坦和螺内酯联合治疗使心脏醛固酮水平恢复正常。本研究首次证明,1型血管紧张素II受体拮抗剂(AT1A)长期治疗可诱导心血管组织局部醛固酮逃逸,而AT1A和螺内酯联合治疗可抑制高血压大鼠的醛固酮逃逸。