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目的肾脏多巴胺和内皮素(ET)系统通过影响近曲小管尿钠排泄在血压调节中发挥重要作用。敲除 ETB 受体基因或 D_3多巴胺受体基因均形成盐敏感性高血压小鼠,并伴有尿钠排泄能力降低;本试验将探索D_3受体和 ETB 受体之间是否存在相互作用以及该作用对 WKY 大鼠尿钠排泄的影响。方法应用 D_3受体激动剂、拮抗剂和 ETB 受体拮抗剂灌注 WKY 大鼠右肾动脉,观察刺激、抑制 D_3、ETB 受体后 WKY 肾功能尤其是尿钠排泄的变化。结果 PD128907刺激 D_3受体后,WKY 尿钠排泄增加,PD128907介导的促尿钠排泄作用可被 D_3受体拮抗剂 GR103691所阻断;ETB 受体拮抗剂 BQ788本身对尿钠排泄无明显影响,但可部分阻断 D_3受体介导的利钠作用。结论 D_3受体的促尿钠排泄作用部分通过 ETB 受体完成。
Purpose The kidneys dopamine and endothelin (ET) systems play an important role in the regulation of blood pressure by affecting urinary sodium excretion of proximal tubules. Knockout ETB receptor gene or D_3 dopamine receptor gene are salt-sensitive hypertensive mice with decreased urinary sodium excretion; this experiment will explore the D_3 receptor and ETB receptor interaction exists between the Effects of Urinary Sodium on Urinary Sodium Excretion in WKY Rats. Methods D_3 receptor agonist, antagonist and ETB receptor antagonist were infused into right renal artery of WKY rats to observe the changes of WKY renal function, especially urinary sodium excretion after stimulation and inhibition of D_3 and ETB receptors. Results After PD128907 stimulated D_3 receptor, WKY increased urinary sodium excretion and PD128907-mediated natriuretic activity was blocked by D_3 receptor antagonist GR103691. ETB receptor antagonist BQ788 itself had no effect on urinary sodium excretion, But can partially block the D_3 receptor mediated sodium function. Conclusions The natriuretic effect of D_3 receptor is partly mediated by ETB receptor.