Zhang Ye, Jose Pedro A, Zeng Chunyu
Contrib Nephrol. 2011;172:63-75. doi: 10.1159/000328684. Epub 2011 Aug 30.
Human essential hypertension and rodent genetic hypertension are associated with increased sodium transport in the renal proximal tubule and medullary thick ascending limb of Henle. The proximal tubule, which secretes endothelin (ET), expresses the ET(B) receptor. Low (nM) concentrations of ET, via the ET(B) receptor, inhibit sodium and water transport and ATP-driven drug secretion in the proximal tubule. In contrast, very low (pM) and high nM concentrations of ET increase renal proximal sodium transport, but the receptor involved remains to be determined. The natriuretic effect of ET(B) receptor stimulation is impaired in spontaneously hypertensive rats, due in part to a defective interaction with D(3) dopamine and angiotensin II type 1 receptors. Impaired ET(B) receptor function in the renal proximal tubule may be important in the pathogenesis of genetic hypertension.
人类原发性高血压和啮齿动物遗传性高血压与肾近端小管及髓袢升支粗段钠转运增加有关。分泌内皮素（ET）的近端小管表达ET（B）受体。低（纳摩尔）浓度的ET通过ET（B）受体抑制近端小管中的钠和水转运以及ATP驱动的药物分泌。相比之下，极低（皮摩尔）和高纳摩尔浓度的ET会增加肾近端钠转运，但所涉及的受体仍有待确定。在自发性高血压大鼠中，ET（B）受体刺激的利钠作用受损，部分原因是与D（3）多巴胺和1型血管紧张素受体的相互作用存在缺陷。肾近端小管中ET（B）受体功能受损可能在遗传性高血压的发病机制中起重要作用。
