Source: Kidney International. Unidade: ICB
Assunto: FISIOLOGIA
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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, v. 70, n. 1, p. 51-59, 2006Tradução . . Disponível em: https://doi.org/10.1038/sj.ki.5000388. Acesso em: 16 nov. 2024.APA
Bailey, M. A., Cantone, A., Yan, Q., MacGregor, G. G., Leng, Q., Amorim, J. B. O., et al. (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.5000388NLM
Bailey MA, Cantone A, Yan Q, MacGregor GG, Leng Q, Amorim JBO, Wang T, Hebert SC, Giebisch G, Malnic G. 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 [Internet]. Kidney International. 2006 ; 70( 1): 51-59.[citado 2024 nov. 16 ] Available from: https://doi.org/10.1038/sj.ki.5000388Vancouver
Bailey MA, Cantone A, Yan Q, MacGregor GG, Leng Q, Amorim JBO, Wang T, Hebert SC, Giebisch G, Malnic G. 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 [Internet]. Kidney International. 2006 ; 70( 1): 51-59.[citado 2024 nov. 16 ] Available from: https://doi.org/10.1038/sj.ki.5000388
