Phenolphthalein- and harmaline-induced disturbances in the transport functions of isolated brush border and basolateral membrane vesicles from rat jejunum and kidney cortex.
Phenolphthalein- and harmaline-induced disturbances in the transport functions of isolated brush border and basolateral membrane vesicles from rat jejunum and kidney cortex.
复制标题
酚酞和骆驼蓬碱引起大鼠空肠和肾皮质分离刷状缘和基底外侧膜囊泡运输功能的紊乱。
DOI：
10.1016/0006-2952(80)90263-4
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发表时间：
1980
影响因子：
5.8
通讯作者：
Faust,RG
中科院分区：
文献类型：
--
作者：
Im,WB;Misch,DW;Powell,DW;Faust,RG
研究了酚酞和骆驼蓬碱对纯化的大鼠空肠和肾皮质刷状缘和基侧膜小泡转运功能的影响。酚酞(0.5 mM)抑制肠刷状缘膜囊泡对Na+-偶联葡萄糖的摄取，但不影响Na+-偶联丙氨酸转运、Na+转运或非Na+-葡萄糖转运。在肾刷状缘膜囊泡中，相同浓度的该药对Na+-偶联葡萄糖摄取无明显影响。然而，在1 mM或更高的浓度下，酚酞使肠和肾小泡都泄漏到这些溶质中。在肠和肾基底外侧膜小泡上，0.5 mM的酚酞显著抑制(Na+-K+)-ATPase活性，但对根素敏感的Na+-非依赖性葡萄糖摄取无影响。在1 mM时，该药物还抑制哇巴因不敏感的ATPase活性。当浓度大于2 mM时，Harmaline不仅抑制肠和肾刷状缘膜囊泡对Na+-偶联葡萄糖和l-丙氨酸的摄取，而且还抑制Na+的转运。然而，该药物既不影响钠离子非依赖性葡萄糖的摄取，也不影响这些膜的一般通透性。Harmaline还抑制肠和肾基底外侧膜囊泡的(Na+-K+)-ATPase活性，但不影响哇巴因不敏感的ATPase。然而，它并不影响这些囊泡对根黄素敏感的钠非依赖性葡萄糖的摄取。这些观察结果表明，骆驼蓬碱对肠和肾刷状缘膜上依赖于Na+和Na+的转运机制具有抑制作用。较低浓度的酚酞选择性地抑制这些膜和基侧膜中的某些运输过程，而较高浓度的酚酞则引起广泛的结构紊乱，可能是通过其对膜的杂化作用。
Phenolphthalein and harmaline were examined with respect to their effects on the transport functions of purified brush border and basolateral membrane vesicles from rat jejunum and kidney cortex. Phenolphthalein (0.5 mM) inhibited Na+-coupledd-glucose uptake by intestinal brush border membrane vesicles without affecting Na+-coupledl-alanine transport, Na+transport or Na+-independentd-glucose transport. In renal brush border membrane vesicles, the same concentration of this drug did not even affect Na+-coupledd-glucose uptake. At a concentration of 1 mM or higher, however, Phenolphthalein rendered both intestinal and renal vesicles leaky to these solutes. In intestinal and renal basolateral membrane vesicles, phenolphthalein at a concentration of 0.5 mM noticeably inhibited (Na+-K+)-ATPase activity, but showed no effect on phloretin-sensitive Na+-independentd-glucose uptake. At 1 mM this drug also inhibited ouabain-insensitive ATPase activity. Harmaline, at concentrations greater than 2 mM, inhibited not only Na+-coupledd-glucose andl-alanine uptake by both intestinal and renal brush border membrane vesicles, but also Na+translocation. The drug, however, affected neither Na+-independentd-glucose uptake nor the general permeability of these membranes. Harmaline also inhibited (Na+-K+)-ATPase activity of intestinal and renal basolateral membrane vesicles without affecting ouabain-insensitive ATPase. It did not influence, however, phloretin-sensitive Na+-independentd-glucose uptake by these vesicles. These observations suggest that harmaline acts as an inhibitor of Na+and Na+-dependent transport mechanisms in intestinal as well as renal brush border membranes. Phenolphthalein at the lower concentration selectively inhibited certain transport processes in these membranes as well as in basolateral membranes, whereas at the higher concentration it caused widespread structural disturbances, possibly through its chaotropic action on membranes.