Our results suggest that endogenous ouabain triggers two different signaling processes. The first, fast process, modulates the activation gating device of the Na V 1.8 channels, thereby reducing their functional activity. The second, slow process, decreases the density of Na V 1.8 channels in the membrane of the primary sensory neuron. We assume that in this case, endogenous ouabain triggers a downstream cascade leading to a decrease in the expression of the SCN10A gene that produces Na V 1.8 channels. It can be concluded that endogenous ouabain, when it interacts with the primary sensory neuron, performs important function of modulating functional activity of Na V 1.8 channels. The practical result of the study was the assumption that the delivery of ouabain as a drug substance to the membrane of a nociceptive neuron in nanomolar concentration should lead to a safe and effective antinociceptive action of this agent at the organismal level.