ANGIOTENSIN-II STIMULATES BOTH NA+-H+ EXCHANGE AND NA+/HCO-3 COTRANSPORT IN THE RABBIT PROXIMAL TUBULE
ANGIOTENSIN-II STIMULATES BOTH NA+-H+ EXCHANGE AND NA+/HCO-3 COTRANSPORT IN THE RABBIT PROXIMAL TUBULE
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DOI：
10.1073/pnas.87.20.7917
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发表时间：
1990-10-01
影响因子：
11.1
通讯作者：
BORON, WF
中科院分区：
文献类型：
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作者：
GEIBEL, J;GIEBISCH, G;BORON, WF
血管紧张素II（AII）是一种强有力的刺激HCO 3-重吸收在大鼠近曲小管在体内。为了确定增加HCO 3-重吸收的离子机制，我们研究了AII对从兔肾浅表肾单位分离的灌注S1近端小管中的管腔Na+-H+交换和基底外侧Na+/HCO 3-共转运的影响。通过从管腔和基底外侧（即浴）溶液中去除Na+并确定Na+仅返回管腔或仅返回浴后细胞内pH（pHi）增加的速率来评估转运蛋白活性。用pH敏感性荧光染料2“，7”-双（2-羧乙基）-5（和6）-羧基荧光素测量pHi。我们发现，基底外侧施用1 nM AII不仅增加了腔Na+-H+交换的速率。3.5-倍，但也增加了基底外侧Na+/HCO 3-共转运的速率。2.5-fold. 5-（n-乙基-N-异丙基）阿米洛利（50 μ M）在AII刺激之前和之后阻断管腔Na+-H+交换，但对基底外侧Na+/HCO 3-共转运没有影响。相反，4，4“-二异硫氰基-2，2”-芪二磺酸盐（50 μ M）在AII前后阻断基底外侧Na+/HCO 3-共转运，但对腔Na+-H+交换没有影响。因此，我们的数据表明，至少在我们的测定条件下，AII独立地刺激负责跨上皮HCO 3重吸收的管腔和基底侧步骤的转运蛋白。
Angiotensin II (AII) is a potent stimulus for HCO3- reabsorption in the rat proximal tubule in vivo. To determine the ionic mechanism of increased HCO3- reabsorption, we have examined the effect of AII on luminal Na+-H+ exchange and basolateral Na+/HCO3- cotransport in perfused S1 proximal tubules isolated from superficial nephrons of the rabbit kidney. Transporter activity was assessed by removing Na+ from both luminal and basolateral (i.e, bath) solutions and determining the rate at which intracellular pH (pHi) increased after Na+ was returned to only the lumen or only the bath. pHi was measured with the pH-sensitive fluorescent dye 2'',7''-bis(2-carboxyethyl)-5(and 6)-carboxyfluorescein. We found that basolateral administration of 1 nM AII not only increased the rate of luminal Na+-H+ exchange .apprxeq. 3.5-fold but also increased the rate of basolateral Na+/HCO3- cotransport .apprxeq. 2.5-fold. 5(n-Ethyl-N-isopropyl)amiloride (50 .mu.M) blocked luminal Na+-H+ exchange before and after stimulation by AII but had no effect on basolateral Na+/HCO3- cotransport. Conversely, 4,4''-diisothiocyanato-2,2''-stilbenedisulfonate (50 .mu.M) blocked basolateral Na+/HCO3- cotransport before and after AII but had no effect on luminal Na+-H+ exchange. Our data thus indicate that, at least under the conditions of our assay, AII independently stimulates the transporters responsible for both the luminal and basolateral steps of transepithelial HCO3- reabsorption.