Cite
Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet.
MLA
Bailey, M. A., et al. “Maxi-K Channels Contribute to Urinary Potassium Excretion in the ROMK-Deficient Mouse Model of Type II Bartter’s Syndrome and in Adaptation to a High-K Diet.” Kidney International, vol. 70, no. 1, July 2006, pp. 51–59. EBSCOhost, https://doi.org/10.1038/sj.ki.5000388.
APA
Bailey, M. A., Cantone, A., Yan, Q., MacGregor, G. G., Leng, Q., Amorim, J. B. O., Wang, T., Hebert, S. C., Giebisch, G., & Malnic, G. (2006). Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter’s syndrome and in adaptation to a high-K diet. Kidney International, 70(1), 51–59. https://doi.org/10.1038/sj.ki.5000388
Chicago
Bailey, M. A., A. Cantone, Q. Yan, G. G. MacGregor, Q. Leng, J. B. O. Amorim, T. Wang, S. C. Hebert, G. Giebisch, and G. Malnic. 2006. “Maxi-K Channels Contribute to Urinary Potassium Excretion in the ROMK-Deficient Mouse Model of Type II Bartter’s Syndrome and in Adaptation to a High-K Diet.” Kidney International 70 (1): 51–59. doi:10.1038/sj.ki.5000388.