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作 者:于长青[1] 石伟彬[1] 杨剑[1] 傅春江[1] 何多芬[1] Laureano D.Asico Pedro A.Jose 曾春雨[1]
机构地区:[1]第三军医大学大坪医院(野战外科研究所)心内科,心血管病研究室,重庆400042 [2]Department of Pediatrics, Georgetown University Medical Center, Washington, DC
出 处:《中华高血压杂志》2008年第6期529-532,共4页Chinese Journal of Hypertension
基 金:国家自然基金资助项目(30470728、30672199);国家科技部973前期研究专项(2008CB517308)
摘 要: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。Objective The dopaminergic and endothelin systems play important roles in the control of blood pressure by regulating sodium transport in the renal proximal tubule(RPT). Deletion of the ETB receptor or D3 receptor gene in rats results in salt-sensitive hypertension with impaired sodium excretion. We investigated inter- action between D3 and ETB receptors and its effect on sodium excretion in Wistar-Kyoto rats. Methods D3 or ETB receptor agonists and/or antagonists were infused selectively into the right kidney of anesthetized WKY rats (WKY). The renal function, especially the sodium excretion, was checked in WKY rats with or without reagent treatment. Results Activation of D3 receptor with D3 receptor agonist (PD128907) increased sodium excretion in WKY rats, which could be blocked by D3 receptor antagonist, GR103691. Although ETB receptor antagonist BQ788, by itself, had no effect on sodium excretion, The D3 receptor-mediated natriuresis was partially blocked by BQ788. Conclusion The natriuretic effect of D3 receptor is partially via ETB receptor in WKY rats.
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