Grünfeld J P, Eloy L
INSERM Unité 90, Hôpital Necker, Paris.
Arch Mal Coeur Vaiss. 1987 Jun;80(6):822-5.
The role of glucocorticoids (Gs) in the regulation of blood pressure has been examined using an antiglucocorticoid, RU 486, at a dose of 20 mg.kg-1 day-1 X 5 days, in male Wistar rats on a low sodium diet. In unanesthetized and chronically catheterized rats, RU 486 administration decreases mean blood pressure (MBP) by approximately 14 mmHg, without altering growth rate or urinary sodium excretion. Corticosterone administration (1 mg.kg-1 day-1) restores MBP nearly to basal level. Glomerular filtration rate evaluated from inulin clearance is unchanged whereas PAH clearance increases and filtration fraction decreases slightly. In anesthetized rats, RU 486 pretreatment decreases MBP, increases cardiac output (radiolabelled microsphere method), and depresses total and renal vascular resistance. In conclusion, endogenous Gs contribute to blood pressure control in salt-restricted rats, possibly by increasing vascular reactivity to catecholamines and angiotensin.
已使用抗糖皮质激素RU 486(剂量为20 mg·kg⁻¹·天⁻¹,连续5天)对低钠饮食的雄性Wistar大鼠进行研究,以探讨糖皮质激素(Gs)在血压调节中的作用。在未麻醉且长期插管的大鼠中,给予RU 486可使平均血压(MBP)降低约14 mmHg,而不改变生长速率或尿钠排泄。给予皮质酮(1 mg·kg⁻¹·天⁻¹)可使MBP几乎恢复到基础水平。根据菊粉清除率评估的肾小球滤过率未改变,而对氨基马尿酸清除率增加,滤过分数略有降低。在麻醉大鼠中,RU 486预处理可降低MBP,增加心输出量(放射性微球法),并降低总血管阻力和肾血管阻力。总之,内源性Gs可能通过增加血管对儿茶酚胺和血管紧张素的反应性,对限盐大鼠的血压控制起作用。