What are the body's responses to maintain water electrolyte?

SODIUM REGULATION:

In healthy individuals, urinary sodium excretion increases when there is an excess of sodium in the body and decreases when there is a sodium deficit. The responses that regulate urinary sodium excretion are initiated mainly by various cardiovascular baroreceptors, such as the kidney that monitor the filtered load of sodium.

The regulation of cardiovascular pressures by baroreceptors also simultaneously achieve regulation of total body sodium. Plasma (sodium) volume is an important determinant of the blood pressures in the veins, cardiac chambers and arteries. Thus, the chain linking total body sodium to cardiovascular pressures is completed., low total-body sodium leads to low plasma volume, hence to low cardiovascular pressure. These low pressures via baroreceptors, initiate reflexes that influences renal arterioles and tubules so as to lower GFR and increase sodium reabsorption. These events decrease sodium excretion, thereby retaining sodium in the body and prevents decrease in plasma volume.

Conversely, an increase in GFR is usually elicited by neuroendocrine inputs when an increased total body sodium level increases plasma volume. This increased GFR contributes to the increased renal sodium loss that returns extracellular volume to normal.

IN CASE OF SODIUM DEPLETION:

The renal sympathetic nerves directly innervate the juxtaglomerular cells, and an increase in the activity of these nerves stimulates renin secretion. Other two inputs for controlling renin release- Intrarenal baroreceptors and the macula densa (contained within the kidneys). Renin  , enzyme secreted by juxtaglomerular cells, splits a small polypeptide, angiotensin 1 from a larger plasma protein angiotensinogen (produced by liver). Angiotensin 1 is a biologically inactive peptide that undergoes further cleavage to form the active agent i.e., angiotensin 2, carried by enzyme angiotensin-converting enzyme (ACE) (found in high conc. on luminal surface of capillary endothelial cells). Angiotensin 2 stimulates secretion of aldosterone. 

Aldosterone, a steroid hormone produced by adrenal cortex stimulates sodium reabsorption by the distal convoluted tubule and the cortical collecting ducts. In the absence of aldosterone, sodium is not reabsorbed but is excreted. 

IN CASE OF EXCESS OF SODIUM

Another controller is Atrial Natriuretic Peptide (ANP), also known as Atrial Natriuretic Factor (ANF)or Hormone (ANH). Cells in the cardiac atria synthesize and secrete ANP. ANP acts on several tubular segments to inhibit sodium reabsorption, it also increases GFR contributing to increased sodium excretion.

ANP also directly inhibits aldosterone secretion, which loads to an increase in sodium excretion. ANP secretion increases because of the expansion of plasma volume that accompanies an increase in  body sodium. The specific stimulus is increased atrial distension. 

WATER REGULATION:

A decreased extracellular fluid volume, due to for example, diarrhea, elicits an increase in aldosterone release via activation of renin-angiotensin system, but this decreased extracellular volume also triggers an increase in vasopressin secretion. The increased vasopressin increases the water permeability of the collecting ducts. More water is passively reabsorbed and less is excreted, so water is retained to help stabilize the extracellular volume. Vasopressin is secreted by posterior pituitary, in response to reflex initiated by several baroreceptors in the cardiovascular system. The baroreceptors decrease their rate of firing when cardiovascular pressure decrease, therefore baroreceptors transmit fewer impulses via afferent neurons and ascending pathway to hypothalamus and the result is increased vasopressin secretion.

Vasopressin increases water permeability by bringing aquaporins to the cell surface. Conversely, increased cardiovascular pressure cause more firing by the baroreceptors, resulting in a decrease in vasopressin secretion.

In some cases, changes in total body water with no corresponding change in total body sodium are compensated for by altering water excretion without altering sodium excretion. Under conditions due predominantly to water gain or loss, the receptors that initiate the reflexes controlling vasopressin secretion are osmoreceptors in the hypothalamus. These receptors are responsive to changes in osmolarity. Deficits of salt and water must eventually be compensated for by ingestion of these substances, because the kidneys cannot create new sodium ions or water. The subjective feeling of thirst is stimulated by an increase in plasma osmolarity and by a decrease in extracellular fluid volume. The brain centers that mediate thirst are located in hypothalamus. 

POTASSIUM REGULATION:

Potassium is freely filterable in the renal corpuscle. Normally, the tubules reabsorb most of this filtered potassium so that very little of  the filtered potassium appears in the urine. However, the cortical collecting ducts can secrete potassium, and changes in potassium excretion are due mainly to changes in potassium secretion by this tubular segment.

During potassium depletion, when the homeostatic response is to minimize potassium loss, there is no potassium secretion by the cortical collecting ducts. Only a small amount of filtered potassium that escapes tubular reabsorption is excreted. In the tubular segment (cortical duct), the K+ pumped into the cell across the basolateral membrane by Na+/K+ ATPases diffuses into the tubular lumen through K+ channels in the luminal membrane. Thus the secretion of K+ by cortical collecting duct is associated with the reabsorption of sodium by this segment.

When a high potassium is ingested, plasma potassium concentration increases, though very slightly , and this drives enhanced basolateral uptake via the Na+/K+ ATPase pumps. Thus, there is an enhanced K+ secretion. And in a low potassium diet or a negative potassium balance, reduces K+ secretion and excretion, thereby helping to reestablish potassium balance.

A second factor linking potassium secretion to potassium balance is the hormone aldosterone, aldosterone enhances the tubular potassium secretion by this tubular potassium secretion by this tubular segment. Aldosterone secreting cells of the adrenal cortex are sensitive to the potassium concentration of the extracellular fluid. So increase K+ levels, directly stimulate the adrenal cortex to produce aldosterone, hence facilitating its enhanced secretion.  

BICARBONATE REGULATION:

Bicarbonate is completely filterable at the renal corpuscles and undergoes significant tubular reabsorption in the proximal tubule, ascending loop of Henle, and in cortical collecting ducts. The kidneys eliminate or replenish hydrogen ions from the body by altering plasma bicarbonate concentration.

CO2 combines with H2O to form H2CO3, a reaction catalyzed by the enzyme carbonic anhydrase. The H2CO3 immediately dissociates to yield H+ and bicarbonate HCO3-. The HCO3- diffuses down its conc. gradient across the basolateral membrane into the interstitial fluid and then into the blood. Simultaneously H+ is secreted into the lumen. Depending on the tubular segment, this secretion is achieved by some combination of primary H+ ATPase pumps, primary H+/K+ ATPase pumps, and Na+/H+ counter transporters. The secreted H+, however is not excreted. Instead it combines in the lumen with a filtered HCO3- and generates CO2 and H2O, both of which can diffuse into the cell and be available for another cycle of hydrogen ion generation. In this manner, no net charge change in plasma bicarbonate concentration has occurred. 

However bicarbonate can be added by renal metabolism of glutamine and excretion of ammonium and by combining H+ with phosphate (HPO42-) rather than by HCO3- (filtered) and getting excreted as H2PO4-.