局部产生的管腔血管紧张素II通过AT1受体对近端肾小管钠重吸收的调节作用。
Modulation by locally produced luminal angiotensin II of proximal tubular sodium reabsorption via an AT1 receptor.
作者信息
Hiranyachattada S, Harris P J
机构信息
Department of Physiology, University of Melbourne, Parkville, Victoria, Australia.
出版信息
Br J Pharmacol. 1996 Oct;119(4):617-8. doi: 10.1111/j.1476-5381.1996.tb15717.x.
The concentration of angiotensin II reported in proximal tubular fluid in anaesthetized rats is considerably higher than in plasma, indicating secretion of this peptide into the tubular lumen. Shrinking split-drop micropuncture was used to examine the effect of endogenous angiotensin on sodium and water absorption in the proximal convoluted tubule. Addition of losartan, a nonpeptide AT1 receptor blocker, to intratubular fluid increased fluid uptake by 15.7 +/- 3.9% (10(-5) M) and 24.7 +/- 9.4% (10(-4) M) whereas the AT2 inhibitor, PD123319 had no effect. We conclude that angiotensin II is secreted into proximal tubular fluid and, in the anaesthetized rat, is maintained at a concentration that inhibits sodium and water transport via AT1 receptors.
麻醉大鼠近端肾小管液中报道的血管紧张素II浓度显著高于血浆中的浓度，这表明该肽分泌到肾小管腔中。采用缩窄微穿刺技术研究内源性血管紧张素对近端曲管钠和水重吸收的影响。向肾小管内液中添加非肽类AT1受体阻滞剂氯沙坦可使液体摄取量增加15.7±3.9%（10⁻⁵ M）和24.7±9.4%（10⁻⁴ M），而AT2抑制剂PD123319则无此作用。我们得出结论，血管紧张素II分泌到近端肾小管液中，在麻醉大鼠中，其浓度维持在通过AT1受体抑制钠和水转运的水平。
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