SERUM SODIUM AND BODY FLUID REGULATION
Oct 15, 2009 5:42:19 GMT 10
Post by Tom Meulman on Oct 15, 2009 5:42:19 GMT 10
SERUM SODIUM AND BODY FLUID REGULATION
It is sodium that is primarily responsible for the level of fluid in the body and the distribution of water between the inside (Intra cellular) and outside (Extra cellular) of the cells.
Problems associated with deficit and excess of sodium reflect this function, deficit-causing dehydration, while excess could cause problems as severe as brain damage.
Cell membranes are relatively impregnable to sodium, but are easily penetrable to water, and any sodium ions that do gain access to the cell interior are actively pushed back into the extra cellular fluid by pumps in the cell membrane.
This pumping action depends on Potassium Ions, and as sodium is pushed out of the cells, potassium is pumped in. In this way, potassium maintains the intracellular pressure.
Since water easily flows between the intracellular (inside the cell) and extra cellular (outside the cell) fluid, concentrations of both these major fluids is always the same.
Normal regulation of body fluid volume also depends up on a balance between water loss and water intake.
If increased drinking is not compensated by increased urine loss, body water must increase, end result over hydration of the cells.
On the other hand, if increased drinking does not compensate urine loss, body water decreases with resulting cellular dehydration.
The stimulation to drink is generated in, what is called the primary thirst centre of the brain, and the basic stimulation for the primary thirst centre is intracellular dehydration.
Stimulation of the primary thirst centre may also be triggered by volume and pressure receptors located in some of the larger blood vessels.
A reduction of 8% in blood volume or pressure can induce thirst and stimulate the release of an anti diuretic hormone (ADH).
While a 2% change in the extra cellular fluid volume will also cause ADH release and cause the kidneys to re-absorb water and concentrate the urine.
In addition to water re-absorption, ADH also increases the re-absorption of Urea.
This is important, as Urea influences the ability of the kidneys to re-absorb water.
However, stimulation of the primary thirst centre is not the only mechanism that determines water intake in normal animals. Food intake as well as exercise also triggers thirst, in anticipation of possible water needs, before any actual cellular deficiencies can occur.
Sodium balance is closely regulated and maintained within narrow limits regardless of large variations in the dietary intake of sodium. Although sodium is excreted from both the gastrointestinal tract and the kidneys, it is the kidneys that primarily regulate sodium balance.
Several factors influence this function; this includes a mineralocorticoid called Aldosterone secreted by the Adrenal Cortex, the volume of blood flow through the kidneys, and the availability of ADH and Urea.
In a normal healthy dog nearly 75% of the fluid that passes through the kidneys is re-absorbed.
Essential to this function are Aldosterone, ADH, Urea, and Sodium.
Anything that affects the available levels of these substances will affect the ability of the kidneys to function normally.
So called acid neutralizers, alkalising diuretics, some infections (viral and bacterial), toxic substances and kidney disease, all reduce the ability of the kidneys to re-absorb water, and causing various levels of dehydration and loss of essential substances, such as potassium.
Low Serum Sodium (Hyponatremia)
Low sodium level can be due to decreased intake or increased excretion of sodium.
Any decrease in the serum sodium concentration following sodium loss is initially corrected by a reduction of both thirst and ADH secretion, reducing fluid intake and increasing urine volume.
In this manner serum sodium concentration is maintained, but at the expense of body fluid volume, causing rapid dehydration.
With progressive sodium loss, extra cellular volume (hydration) keeps on reducing, and at a critical point, (8% reduction in blood volume) blood vessel volume receptors stimulate extreme thirst and ADH production, causing a water gain and a rapid decrease in serum sodium concentration.
Hyponatremia is characterized by signs of dehydration, decreased skin pliability, weak pulse, and the increased production of urine with low specific gravity (Polyuria).
High Serum Sodium (Hypernatremia)
High serum sodium causes water to transfer out of the brain into the extra cellular fluid, resulting in severe weakness and coma.
Severe heatstroke, excessive sodium administration, and kidney failure may also cause high serum sodium.
This is life threatening, and requires immediate and appropriate therapy, which will depend on the degree of dehydration.
It is sodium that is primarily responsible for the level of fluid in the body and the distribution of water between the inside (Intra cellular) and outside (Extra cellular) of the cells.
Problems associated with deficit and excess of sodium reflect this function, deficit-causing dehydration, while excess could cause problems as severe as brain damage.
Cell membranes are relatively impregnable to sodium, but are easily penetrable to water, and any sodium ions that do gain access to the cell interior are actively pushed back into the extra cellular fluid by pumps in the cell membrane.
This pumping action depends on Potassium Ions, and as sodium is pushed out of the cells, potassium is pumped in. In this way, potassium maintains the intracellular pressure.
Since water easily flows between the intracellular (inside the cell) and extra cellular (outside the cell) fluid, concentrations of both these major fluids is always the same.
Normal regulation of body fluid volume also depends up on a balance between water loss and water intake.
If increased drinking is not compensated by increased urine loss, body water must increase, end result over hydration of the cells.
On the other hand, if increased drinking does not compensate urine loss, body water decreases with resulting cellular dehydration.
The stimulation to drink is generated in, what is called the primary thirst centre of the brain, and the basic stimulation for the primary thirst centre is intracellular dehydration.
Stimulation of the primary thirst centre may also be triggered by volume and pressure receptors located in some of the larger blood vessels.
A reduction of 8% in blood volume or pressure can induce thirst and stimulate the release of an anti diuretic hormone (ADH).
While a 2% change in the extra cellular fluid volume will also cause ADH release and cause the kidneys to re-absorb water and concentrate the urine.
In addition to water re-absorption, ADH also increases the re-absorption of Urea.
This is important, as Urea influences the ability of the kidneys to re-absorb water.
However, stimulation of the primary thirst centre is not the only mechanism that determines water intake in normal animals. Food intake as well as exercise also triggers thirst, in anticipation of possible water needs, before any actual cellular deficiencies can occur.
Sodium balance is closely regulated and maintained within narrow limits regardless of large variations in the dietary intake of sodium. Although sodium is excreted from both the gastrointestinal tract and the kidneys, it is the kidneys that primarily regulate sodium balance.
Several factors influence this function; this includes a mineralocorticoid called Aldosterone secreted by the Adrenal Cortex, the volume of blood flow through the kidneys, and the availability of ADH and Urea.
In a normal healthy dog nearly 75% of the fluid that passes through the kidneys is re-absorbed.
Essential to this function are Aldosterone, ADH, Urea, and Sodium.
Anything that affects the available levels of these substances will affect the ability of the kidneys to function normally.
So called acid neutralizers, alkalising diuretics, some infections (viral and bacterial), toxic substances and kidney disease, all reduce the ability of the kidneys to re-absorb water, and causing various levels of dehydration and loss of essential substances, such as potassium.
Low Serum Sodium (Hyponatremia)
Low sodium level can be due to decreased intake or increased excretion of sodium.
Any decrease in the serum sodium concentration following sodium loss is initially corrected by a reduction of both thirst and ADH secretion, reducing fluid intake and increasing urine volume.
In this manner serum sodium concentration is maintained, but at the expense of body fluid volume, causing rapid dehydration.
With progressive sodium loss, extra cellular volume (hydration) keeps on reducing, and at a critical point, (8% reduction in blood volume) blood vessel volume receptors stimulate extreme thirst and ADH production, causing a water gain and a rapid decrease in serum sodium concentration.
Hyponatremia is characterized by signs of dehydration, decreased skin pliability, weak pulse, and the increased production of urine with low specific gravity (Polyuria).
High Serum Sodium (Hypernatremia)
High serum sodium causes water to transfer out of the brain into the extra cellular fluid, resulting in severe weakness and coma.
Severe heatstroke, excessive sodium administration, and kidney failure may also cause high serum sodium.
This is life threatening, and requires immediate and appropriate therapy, which will depend on the degree of dehydration.