Non-pharmacological aspects of blood pressure management: what are the data?  S. Susan Hedayati, Essam F. Elsayed, Robert F. Reilly  Kidney International  Volume 79, Issue 10, Pages 1061-1070 (May 2011) DOI: 10.1038/ki.2011.46 Copyright © 2011 International Society of Nephrology Terms and Conditions

Figure 1 Illustration of a model of sodium (Na+) retention causing hypertension in a state of dietary potassium (K+) deficiency, mediated by WNK1. During K+ depletion, to maintain K+ levels, ROMK is downregulated (by endocytosis of ROMK). This downregulation is mediated by an increase in the ratio of L-WNK1 to KS-WNK1 in the kidney, which decreases renal K+ secretion to conserve K+, but also enhances renal Na+ reabsorption via ENaC and NCC, resulting in Na+ retention and hypertension. Adapted from Huang et al.33 Cl−, chloride; ENaC, epithelial sodium channel; Na+, sodium; NCC, Na+/Cl− cotransporter; ROMK, renal outer medullary potassium channel; WNK1, with no lysine kinase 1; KS-WNK1, kidney-specific WNK1; L-WNK1, long WNK1. Kidney International 2011 79, 1061-1070DOI: (10.1038/ki.2011.46) Copyright © 2011 International Society of Nephrology Terms and Conditions