Smith J B, Brock T A
J Cell Physiol. 1983 Mar;114(3):284-90. doi: 10.1002/jcp.1041140306.
Angiotensin peptides (AI, AII, AIII) increased the rate of Na+ accumulation by smooth muscle cells (SMC) cultured from rat aorta. The stimulatory effect of AII on Na+ uptake was observed when Na+ exodus via the Na+/K+ pump was blocked either by ouabain or by the removal of extracellular K+. AII was at least ten times more potent than AIII and about 100 times more potent than AI in stimulating Na+ uptake. Saralasin had little effect on Na+ uptake by itself but almost completely blocked the increase caused by AII. The stimulation of net Na+ entry by AI, but not AII, was prevented by protease inhibitors. The stimulation of Na+ uptake was almost completely blocked by amiloride. Tetrodotoxin, which prevented veratridine from increasing Na+ uptake, had no effect on the response to AII. Angiotensin increased the rate of ouabain-sensitive 86Rb+ uptake (Na+/K+ pump activity) but had no effect on ouabain-sensitive ATPase activity in frozen-thawed SMC or in microsomal membranes isolated from cultured SMC. The stimulation of ouabain-sensitive 86Rb+ uptake by AII was blocked by saralasin. Omitting Na+ from the external medium prevented AII from increasing 86Rb+ uptake. AII had no effect on cell volume or cyclic AMP levels in the cultured SMC. These results suggest that angiotensin peptides activate an amiloride-sensitive Na+ transporter which supplies the Na+/K+ pump with more Na+, its rate-limiting substrate.
血管紧张素肽（AI、AII、AIII）可提高从大鼠主动脉培养的平滑肌细胞（SMC）的Na⁺蓄积速率。当通过哇巴因或去除细胞外钾来阻断经Na⁺/K⁺泵的Na⁺外流时，可观察到AII对Na⁺摄取的刺激作用。在刺激Na⁺摄取方面，AII的效力至少是AIII的10倍，约为AI的100倍。沙拉新本身对Na⁺摄取几乎没有影响，但几乎完全阻断了AII引起的增加。蛋白酶抑制剂可阻止AI（而非AII）对净Na⁺内流的刺激。氨氯吡咪几乎完全阻断了Na⁺摄取的刺激作用。河豚毒素可阻止藜芦碱增加Na⁺摄取，但对AII的反应没有影响。血管紧张素增加了哇巴因敏感的⁸⁶Rb⁺摄取速率（Na⁺/K⁺泵活性），但对冻融的SMC或从培养的SMC分离的微粒体膜中的哇巴因敏感的ATP酶活性没有影响。AII对哇巴因敏感的⁸⁶Rb⁺摄取的刺激作用被沙拉新阻断。从外部培养基中去除Na⁺可阻止AII增加⁸⁶Rb⁺摄取。AII对培养的SMC中的细胞体积或环磷酸腺苷水平没有影响。这些结果表明，血管紧张素肽激活了一种氨氯吡咪敏感的Na⁺转运体，该转运体为Na⁺/K⁺泵提供更多的Na⁺，即其限速底物。
