Eklöf A C
Department of Woman and Child Health, Karolinska Institute, Stockholm, Sweden.
Acta Physiol Scand. 1997 Aug;160(4):311-4. doi: 10.1046/j.1365-201X.1997.00166.x.
Dopamine produced in the kidney acts as a natriuretic hormone by inhibiting tubular Na+,K+-ATPase activity. Previous in vitro studies have shown that Na+,K+-ATPase activity in the proximal tubule is inhibited by a synergistic action of dopamine 1 (DA1) and dopamine 2 (DA2) receptors. This in vivo study, performed on rats, investigates whether the natriuretic response to DA requires a synergistic action of DA1 and DA2 receptors. The DA1 agonist, fenoldopam, significantly increased urinary sodium excretion, but there was no increase in sodium excretion when a DA1 agonist was given together with a DA2 antagonist. Neither DA1 nor DA2 antagonists had any influence on sodium excretion. The natriuretic response to fenoldopam was also significantly attenuated after the administration of benserazide, which inhibits aromatic acid decarboxylase and thereby suppresses the endogenous production of dopamine. In conclusion, the natriuretic effect of dopamine depends on the activation of both DA1 and DA2 receptors. The DA2 receptor appears to be constitutively activated by endogenous dopamine.
肾脏产生的多巴胺通过抑制肾小管钠钾ATP酶活性，起到利钠激素的作用。此前的体外研究表明，多巴胺1（DA1）受体和多巴胺2（DA2）受体的协同作用可抑制近端小管中的钠钾ATP酶活性。本项在大鼠身上进行的体内研究，探究了多巴胺的利钠反应是否需要DA1和DA2受体的协同作用。DA1激动剂非诺多泮显著增加尿钠排泄，但当DA1激动剂与DA2拮抗剂合用时，钠排泄量并未增加。DA1拮抗剂和DA2拮抗剂对钠排泄均无影响。给予抑制芳香酸脱羧酶从而抑制内源性多巴胺生成的苄丝肼后，非诺多泮的利钠反应也显著减弱。总之，多巴胺的利钠作用取决于DA1和DA2受体的激活。DA2受体似乎被内源性多巴胺持续激活。
