What sets the plasma sodium concentration
Concentration is the amount of solute divided by the volume of solution, so a first answer is that the plasma sodium concentration depends on the amount of sodium ion in the blood and the amount of extracellular fluid (ECF). Written out, this is sodium concentration = [Na]/ECF.
That first answer is incomplete, because sodium is not the only solute that matters. Sodium and its anions are the main solutes of the ECF, while potassium is the main solute of the intracellular fluid (ICF). Because the cell membrane is permeable to water, the ICF and the ECF settle at the same osmolality, the concentration of dissolved solute in a fluid. If a large amount of potassium is added to the plasma, it moves into the cells and raises intracellular osmolality; water then shifts from the ECF into the ICF to equalise the two, and that loss of ECF water raises the plasma sodium concentration. So plasma sodium depends on more than the sodium and water in the plasma: it depends on the exchangeable (disposable) sodium, the exchangeable potassium, and the total body water. Edelman expressed this as:
Here $Na_e$ and $K_e$ are the exchangeable sodium and potassium, and $TBW$ is the total body water.
What controls the sodium content of the ECF
Because the amount of sodium in the ECF is one of the things that sets the plasma sodium concentration, the next question is what controls it. Three systems regulate how much sodium the ECF holds. The renin–angiotensin–aldosterone system (RAAS) promotes sodium retention. The natriuretic peptides, such as atrial natriuretic peptide (ANP), are released when a rising blood volume stretches the atria and promote sodium excretion. The sympathetic nervous system also takes part in the control of sodium handling.
Steady state
RAAS and the natriuretic peptides pull in opposite directions, and for any ion excreted into the urine there is a protective mechanism called steady state that keeps the result stable. It means that after a change in the intake or the excretion of an ion that the kidney reabsorbs, only a few days are needed to bring intake and excretion back into balance.
Primary aldosteronism is a useful example, because it tests the idea. Excess aldosterone retains sodium, which might be expected to produce permanent hypernatremia, but it does not. Several mechanisms control the balance of the same ion, and after only a few days, in this case less than 10, atrial natriuretic peptide rises and excretes the sodium that aldosterone retained, so the balance is restored.
Together, these systems and the steady state hold the sodium content of the ECF stable. The plasma sodium concentration, though, also reflects water movement across cell membranes, and that depends on how solute concentration is measured and which solutes are counted.