期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1982
卷号：79
期号：5
页码：1438-1442
DOI：10.1073/pnas.79.5.1438
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Angiotensin markedly altered the Na+ permeability of smooth muscle cells cultured from explants of rat aorta. The rate of net Na+ uptake was followed in the presence of ouabain in order to block Na+ efflux via the Na+/K+ pump. Angiotensin II (AII) or angiotensin III (AIII) increased net Na+ uptake by about 3-fold. Maximal stimulation of Na+ uptake was produced by about 10 nM AII. Bradykinin and the angiotensin antagonist [Sar1, Ileu5, Ala8]AII had no significant effect on net Na+ uptake. Angiotensin also enhanced the activity of the Na+/K+ pump, which was assayed by following the rate of ouabain-sensitive 86Rb+ uptake by the cells. AII and AIII nearly doubled ouabain-sensitive 86Rb+ uptake, but bradykinin, norepinephrine, and [Sar1, Ileu5, Ala8]AII had no effect. In the presence of ouabain, 86Rb+ uptake was not significantly affected by AII or AIII, indicating that angiotensin did not alter passive permeability to Rb+. Loading the cells with Na+, either by incubation in K+-free medium or exposure to the Na+-selective ionophore monensin, markedly increased ouabain-sensitive 86RB+ uptake. This result indicates that the activity of the Na+/K+ pump is limited by the low level of Na+ that is normally in the cells. AII had no effect on the activity of the Na+/K+ pump in Na+-loaded cells. These results suggest that AII or AIII stimulates the Na+/K+ pump in cultured aortic muscle cells by increasing its Na+ supply.
