Mineralocorticoid blockade reduces vascular injury in stroke prone hypertensive rats
Mineralocorticoid blockade reduces vascular injury in stroke prone hypertensive rats
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DOI：
10.1161/01.hyp.31.1.451
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发表时间：
1998-01-01
期刊：
影响因子：
8.3
通讯作者：
Stier, CT
中科院分区：
文献类型：
--
作者：
Rocha, R;Chander, PN;Stier, CT
慢性治疗的盐水饮用中风倾向的自发性高血压大鼠（SHRSP）的药物，干扰血管紧张素II（Ang II）的形成或行动，防止中风和肾血管损伤的发展。血管紧张素II，除了其直接的血管效应，刺激合成和释放的醛固酮。为了评估醛固酮在这些大鼠病理变化发展中的作用，我们将含有200 mg盐皮质激素受体拮抗剂螺内酯的缓释颗粒植入14只7.5周龄的SHRSP中，8只SHRSP同窝仔接受安慰剂颗粒。在研究期间（3至4周），两组之间的收缩压（SBP）没有差异。螺内酯并没有增加水和电解质的排泄。所有安慰剂治疗的SHRSP均出现明显的蛋白尿（150 ± 6 mg/d），而螺内酯治疗的SHRSP的尿蛋白排泄（UPE）平均为39 ± 9 mg/d（P
Chronic treatment of saline-drinking stroke-prone spontaneously hypertensive rats (SHRSP) with agents that interfere with the formation or actions of angiotensin II (Ang II) prevents the development of stroke and renal vascular damage. Ang II, in addition to its direct vascular effects, stimulates the synthesis and release of aldosterone. To assess the role of aldosterone in the development of pathologic changes in these rats, we implanted time-release pellets containing 200 mg of the mineralocorticoid receptor antagonist, spironolactone, into 14 SHRSP at 7.5 weeks of age, Eight SHRSP littermates received placebo pellets. Over the period of study (3 to 4 weeks), systolic blood pressure (SBP) was not different between the groups. Spironolactone did not enhance water and electrolyte excretion. All placebo-treated SHRSP developed marked proteinuria (150+/-6 mg/d) whereas in spironolactone-treated SHRSP, urinary protein excretion (UPE) averaged 39+/-9 mg/d (P