Physiology of body fluidsBody Fluids Compartments:

Water comprised about 70% of the weight of most vertebrates, is distributed in the :-

• 1-intracellular(ICF): fluid inside the cells. 2/3 volume of fluids in body(15% of body weight)

• 2- extracellular (plasma and interstitial) (ECF): fluid outside the cells.1/3 volume of fluids in body(40% of body weight)

• 3- transcellular (alimentary tract, urine, synovial fluid) (5% of body weight)

:

The electrolyte concentrations , pH, and the osmolality of intracellular and extracellular fluids must be regulated . The process of regulating the concentration of water and mineral salts in the body fluid is called osmoregulation, the animal cell has always to be surrounded by an isotonic solution. Osmoregulation of the extracellular fluid is achieved by regulated addition and subtraction of free water from the extracellular fluid, thus diluting or concentrating the already present electrolytes. via adding or removing free water from the ECF.

According to the differences of solutes concentration , extracellular solutions will be differ in their osmolality and classify in to 3 types

Isotonic- Means having the same concentration of solutes so it will not affect the cell.

Hypotonic- Means a solution with low solute concentration, so when a cell is placed in a hypotonic solution, it takes up water and swells and may burst.

Hypertonic- Means a solution with more concentration, i.e more solutes. For example, if a cell is placed in a hypertonic solution, it will shrink in size as water moves from hypertonic to hypotonic.

• These processes are regulated by means of negative feedback mechanism control circuits which sense the extracellular fluid osmolarity and then coordinate free water addition and subtraction in an effort to maintain relatively stable values of osmolarity. When ECF osmolarity rises excessively, these mechanisms promote addition of free water to the ECF, thus reducing ECF osmolarity. In contrast, when ECF osmolarity drops excessively, these processes enhance water loss from the extracellular fluid, thus returning ECF osmolarity to its set point.This organization is work in a reflex behavior,

\There are receptors and other systems in the body that detect a decreased volume or an increased osmolite

concentration. They signal to the central nervous system, where central processing succeeds. Some sources,therefore, distinguish "extracellular thirst" from "intracellular thirst", where extracellular thirst is thirst generated by decreased volume and intracellular thirst is thirst generated by increased osmolite concentration

Hypothalmic centers:Clusters of cells (osmoreceptors) in the organum vasculosum of the lamina terminalis (OVLT) and subfornical organ (SFO), which lie outside of the blood brain barrier can detect the concentration of blood plasma and the presence of angiotensin II in the blood.

Two types:Hypothalmic Volumetric thirst: Decreased volumeThe loss of blood volume is detected by cells in the kidneys and triggers thirst for both water and salt via the renin-

angiotensin system.Feedback signals that inhibit the thirst centers include:

Moistening of the mucosa of the mouth and throatActivation of stomach and intestinal stretch receptors

Hypothalamic Osmometric thirst: Cellular dehydration and osmoreceptor Stimulation trigger or inhibit ADH release Vasopressin (arginine vasopressin, AVP; antidiuretic hormone, ADH) is a peptide hormone formed in thehypothalamus, then transported via axons to, and released

from, the posterior pituitary into the blood ..Factors that specifically trigger ADH release include prolonged fever; excessive sweating, vomiting, or

diarrhea; severe blood loss; and traumatic burns. ADH promote water reabsorption in collecting ducts . Low ADH levels produce dilute urine and reduced volume of body fluids. High ADH levels produce concentrated urine. AVP has two principle sites of action: the kidney and blood vessels.

The primary function of AVP in the body is to regulate extracellular fluid volume by affecting renal handling of water This increases blood volume, cardiac output and arterial pressure.

A secondary function of AVP is vasoconstriction

factors influence on AVP release• There are several mechanisms regulating the release of AVP, the most

important of which are the following:• Hypovolemia, as occurs during hemorrhage and dehydration, results in a

decrease in atrial pressure. Specialized stretch receptors within the atrial walls and large veins (cardiopulmonary baroreceptors) entering the atria decrease their firing rate when there is a fall in atrial pressure. Afferent nerve fibers from these receptors synapse within the nucleus tractus solitarius of the medulla, which sends fibers to the hypothalamus, a region of the brain that controls AVP release by the pituitary. Atrial receptor firing normally inhibits the release of AVP by the posterior pituitary. With hypovolemia or decreased central venous pressure, the decreased firing of atrial stretch receptors leads to an increase in AVP release.

• Hypotension, which decreases arterial baroreceptor firing, leads to enhanced sympathetic activity that increases AVP release.

• Hypothalamic osmoreceptors sense extracellular osmolarity and stimulate AVP release when osmolarity rises, as occurs with dehydration.

• Angiotensin II receptors located in a region of the hypothalamus regulate AVP release – an increase in angiotensin II simulates AVP release.

• Peripheral reseptors:• Cardiopulmonary baroreceptors: Baroreceptors alert the brain of increases in

blood volume (hence increased blood pressure)– Sympathetic nervous system impulses to the kidney

– juxtaglomerular cells (intrarenal baroreceptors) and the macula densa: The renin-angiotensin mechanism triggers the release of aldosterone. This is mediated by juxtaglomerular apparatus, which releases renin in response to:• Sympathetic nervous system stimulation• Decreased filtrate osmolality• Decreased stretch due to decreased blood pressure

– Renin catalyzes the production of angiotensin II, which prompts aldosterone release

– Adrenal cortical cells are directly stimulated to release aldosterone by elevated K+ levels in the ECF

– Aldosterone brings about its effects (diminished urine output and increased blood volume) slowly

• Atrial Stretch receotors

• Atrial Natriuretic Peptide (ANP) • An additional mechanism involved in the regulation of Na+ levels

involves the hormone atrial natriuretic peptide (ANP). This hormone is synthesized by cells in the atrium of the heart, and is released in response to distension of the atria, in other words, when plasma volume increases. The effect of ANP is to increase natriuresis, that is the excretion of Na+ in the urine. ANP increases natriuresis by increasing GFR and decreasing Na+ reabsorption. ANP works to oppose the effects of the renin-angiotensin-aldosterone system, preventing plasma overload by preventing excessive Na+ levels in the body

• Influence of Other Hormones on Sodium Balance– Estrogens:

• Enhance NaCl reabsorption by renal tubules• May cause water retention during menstrual cycles• Are responsible for edema during pregnancy

– Progesterone:• Decreases sodium reabsorption• Acts as a diuretic, promoting sodium and water loss

– Glucocorticoids - enhance reabsorption of sodium and promote edema

Role of Aldosteronein ECF regulation

The principal regulator of Na+ reabsorption is the steroid hormone aldosterone, which is produced in the zona glomerulosa of the adrenal cortex. Aldosterone, like all steroid hormones, works as a transcription factor to alter gene expression in cells. Aldosterone works in the cells of the cortical collecting duct, depicted at left. Na+ reabsorption in this part of the renal tubule accounts for only 2% of total Na+ reabsorption, but this is the site where regulation of Na+ balance occurs.

What is the effect of aldosterone? Aldosterone saves salt. It works to increase Na+reabsorption by promoting the expression of all the channels and pumps depicted in the figure.