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Figure 1: Dietary K+ stimulates splanchnic receptors and causes aldosterone release which acts on principal cells of late distal convoluted tubule and cortical collecting duct that stimulates epithelial sodium channel which maintains electronegative environment by Na intake, favoring K+ secretion. It also stimulates 3Na+–2K+ ATPase, the renal outer medullary potassium and with-no-lysine kinase 4 channels that inhibit Na+–Cl cotransporter in early distal convoluted tubule increasing delivery of Na, Cl in late distal convoluted tubule and cortical collecting duct hence providing substrate for epithelial sodium channel, increasing flow of urine that washes locally secreted K+ favoring more secretion. K+ directly increases expression of 3Na+–2K+ ATPase, the renal outer medullary potassium, epithelial sodium channel, and K+ maxi conductance channels

Figure 1: Dietary K<sup>+</sup> stimulates splanchnic receptors and causes aldosterone release which acts on principal cells of late distal convoluted tubule and cortical collecting duct that stimulates epithelial sodium channel which maintains electronegative environment by Na intake, favoring K<sup>+</sup> secretion. It also stimulates 3Na<sup>+</sup>–2K<sup>+</sup> ATPase, the renal outer medullary potassium and with-no-lysine kinase 4 channels that inhibit Na<sup>+</sup>–Cl<sup>−</sup> cotransporter in early distal convoluted tubule increasing delivery of Na, Cl in late distal convoluted tubule and cortical collecting duct hence providing substrate for epithelial sodium channel, increasing flow of urine that washes locally secreted K<sup>+</sup> favoring more secretion. K<sup>+</sup> directly increases expression of 3Na<sup>+</sup>–2K<sup>+</sup> ATPase, the renal outer medullary potassium, epithelial sodium channel, and K<sup>+</sup> maxi conductance channels