Figure 2.

Image demonstrating potential mechanisms relating how altered Na⁺/K⁺ATPase (as coded byATP1A2)function could be related to stroke risk. Decreased Na⁺/K⁺ ATPase activity leads to: altered ionic (Na⁺, K⁺) gradients resulting in excess intracellular Ca²⁺ (Danbolt 2001); impaired K⁺ channel-mediated membrane repolarization (Luo et al. 2004; Matsuda et al. 2001), and; elevated glutamate concentrations at the synaptic cleft (Rose et al. 2009). Elevated homocysteine has been shown to decrease Na⁺/K⁺ ATPase function (Machado et al. 2011; Streck et al. 2002).