Murphy M B, Bass A S, Goldberg L I
Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637.
Am J Physiol. 1988 Sep;255(3 Pt 2):F494-9. doi: 10.1152/ajprenal.1988.255.3.F494.
This study examined whether the renal effects of atrial natriuretic factor (ANF) are mediated by dopamine1 (DA1) receptor activation. Intravenous infusion of low-dose ANF (0.0025 micrograms.kg-1.min-1) in euvolemic, pentobarbital sodium-anesthetized male mongrel dogs enhanced urine flow (V) by 71 +/- 14% (mean +/- SE) and urinary sodium excretion (UNaV) by 457 +/- 172% (P less than 0.05). Renal blood flow (RBF) was unchanged. Administration of pharmacological doses of ANF (0.1 microgram.kg-1.min-1) into the renal artery in volume-expanded dogs increased RBF by 26 +/- 6, V by 56 +/- 15, and UNaV by 101 +/- 42%. The selective DA1 receptor antagonist SCH-23390 (0.5 microgram.kg-1.min-1 iv) did not affect the response to ANF at either dose. The selective DA1 agonist, fenoldopam, increased RBF by 45 +/- 3, V by 94 +/- 27, and UNaV by 61 +/- 15% in volume-expanded dogs. With SCH-23390, fenoldopam increased RBF by only 16 +/- 6% whereas V and UNaV decreased by 16 +/- 10 and 17 +/- 10%, respectively. Accordingly, the failure of DA1 receptor-blocking doses of SCH-23390 to antagonize the response to ANF, at pharmacological or physiological doses, indicates that the renal effects of ANF, in the dog, are independent of DA1 receptor activation.
本研究检测了心房利钠因子（ANF）的肾脏效应是否由多巴胺1（DA1）受体激活介导。在戊巴比妥钠麻醉的血容量正常雄性杂种犬中静脉输注低剂量ANF（0.0025微克·千克⁻¹·分钟⁻¹），使尿流量（V）增加了71±14%（平均值±标准误），尿钠排泄量（UNaV）增加了457±172%（P<0.05）。肾血流量（RBF）未改变。对血容量扩充的犬经肾动脉给予药理剂量的ANF（0.1微克·千克⁻¹·分钟⁻¹），使RBF增加26±6，V增加56±15，UNaV增加101±42%。选择性DA1受体拮抗剂SCH - 23390（0.5微克·千克⁻¹·分钟⁻¹静脉注射）对任一剂量的ANF反应均无影响。选择性DA1激动剂非诺多泮使血容量扩充犬的RBF增加45±3，V增加94±27，UNaV增加61±15%。使用SCH - 23390时，非诺多泮仅使RBF增加16±6%，而V和UNaV分别降低16±10%和17±10%。因此，在药理或生理剂量下，DA1受体阻断剂量的SCH - 23390未能拮抗对ANF的反应，表明在犬中ANF的肾脏效应独立于DA1受体激活。
