These contemporary theories on the mechanistic disturbances that can cause salt sensitivity fit within the unifying conceptual framework shown in Figure 3. These theories do not depend on the assumption that in response to increases in salt intake, salt-sensitive individuals usually undergo greater increases in sodium retention and cardiac output than salt-resistant normotensive controls. *Note that oxidative stress has been proposed to play a role in many of the theories of salt-sensitivity listed here. Abbreviations: ADMA, asymmetrical dimethylarginine; ENaC, epithelial sodium channel; EnNaC, endothelial ENaC; TGF-β, transforming growth factor-β.