Answer:
When there is a high dietary intake of potassium (K+), there is a higher concentration of K+ in the extracellular fluid (ECF) which causes the cell membrane to depolarize. This could lead to hyperkalemia, which is a serious condition that can lead to cardiac arrhythmia, muscle weakness, and even death.
The Na-Cl cotransporter (NCC) plays a key role in the regulation of blood pressure by reabsorbing Na+ in the distal tubules of the kidneys. The NCC is regulated by the renin-angiotensin-aldosterone system (RAAS) and aldosterone increases reabsorption of Na+ through the NCC.
However, a high K+ intake can inhibit the actions of the RAAS, reducing aldosterone secretion and, therefore, reducing the reabsorption of Na+ through the NCC. This leads to increased Na+ excretion in the urine, which helps decrease blood pressure.
In addition, the increased excretion of Na+ will further limit any potential increases in serum potassium concentrations, reducing the chances of developing hyperkalemia. Therefore, the effect of K+ on NCC can simultaneously prevent hyperkalemia and promote increased Na+ excretion, leading to modulation of blood pressure.