Moistening tissues (eyes, mouth, nose)

Protects organs/tissues (cushion)

Regulation of body temperature (sweating)

Lubrication of joints

Elimination of feces

Delivery vehicle for nutrients and oxygen

Flushing out waste/toxins (kidney, liver)

Intravascular fluid must be regulated to ensure normal heart function

Low blood volume can lead to heart failure via hypervolemia <- can be counteracted by vasoconstriction

Thirst (intake)

Water Loss (output)

Both are very tightly regulated and work together

Intracellular depletion of water (cytoplasm) -> osmotic thirst

Makes up 67% of body fluid

Extracellular depletion of water (interstitial, intravascular, and cerebrospinal fluid) -> hypovolemic thirst

Makes up 33% of body fluid

Detection of changes in osmolality (negative feedback)

Detection of chnages in blood volume

Mechanism to correct any inbalances

Osmotic pressure

Starling equilibrium: oncotic pressure and hydrostatic pressure

Interstitial fluid is plams free, water will be "pulled" into the vasculature which is full of proteins.

Ions (ie. Na+) are not affected and can travel to maintain homeostasis

Hypertonic body fluids -> osmometric thirst

Dec. in blood volume -> volumetric thirst

Water: taken up by dehydrated cells, little effect on blood volume, water can move easily between compartments

Saline: not taken up by dehydrated cells, only affects volume of extracellular body fluid not intracellular osmolarity

Osmotic thirst due to hypertonic interstitial fluid

Volemic thirst (aka hypovolemic thirst) due to low blood volume (hemorrhaging)

Simple dehydration: deprivation of water plus continuous water loss via skin/breathing

High salt meal: hypertonic vascular, interstitial, and intracellular fluid; excess water (and sodium) drwan into vasculare is excreted by kidney; blood volume is unaffected

Specialized neurons whose firing rate is affeted by the level of hydration, increase in firing rate when water loss causes decrease in cell volume

Hyertonic interstitial fluid causes osmosis of water out of osmoreceptors

OVLT: organum vasculosum of the lamina terminalis

SON: supraoptic nucleus

Direct: activation of neural circuits mediating thirst

Indirect: inc. release of vasopressin from posterior pituitary

Unbound to plasma proteins

~5-15 minutes, quickly degraded by peptidases

V1-R: Gq mediated activation of PLC

V2-R: G-alpha-s mediated activation of AC

V3-R: Gq mediated activation of PLC

Regulates reabsorption of water in distal tubule of kidney nephron

Aquaporins in the nephron allow for reabsorption of water and exretion of concentrated urine.

Filtered fluid flows into collecting ducts into the bladder

Blood returns to circulation via the renal vein

Vasopressing causes the reuptake of water, concentrating the urine

Vasopressin increases aquaporin expression on cell surface of distal tube -> water passes through aquaporins to exit distal tube and re-enter interstitium

Reuces renal excretion of water - ADH

Stimulates constriction of blood vessels - helps to support BP during mild dec. in intravascular fluid volume

Rapid changes in plasma osmolarity - rapid inc. lead to exaggerated release

During the act of drinking - suppresses vasopressin release through afferent pathways originating in oropharynx

Pregnancy - osmotic threshold for vasopressin is lowered

Dec. in BP leads to exponential inc. in vasopressin release

Reduction in circulating blood vollume stimulates vasopressin release - baroreceptor input through NTS

Kidneys produce large volumes of dilute urine.

Neurogenic - deficiency of vasopressin

Nephrogenic - insensitivity to vasopressin (defective receptors)

Interneurons are inhibitory

Project to vasopressinergic neurons of SON and PVN and inhibit vasopressin neurons with normal osmoreceptor volume

Extend dendrites around the osmoreceptor and act as mechanoreceptors

Dec in blood plasma:

- blood loss: loss of water and sodium

- vomiting

- diarrhea

*does not require change in tonicity of plasma

Kidneys: juxtaglomerular cells

Heart and large blood vessels: atrial baroreceptors

JG cells are located at the end of the ascending loop of Henle and detect a drop in BP (probably through intrarenal baroreceptors) -> release renin due to dec. BP or dec plasma Na+ level

JG cells receive input from SNS -> hypotension and hypovolemia cause NE release -> JG cells express beta-adrenergic receptors -> binding of NE causes renin release

AT1 and AT2 receptors

AT1 has most effect on fluid balance

In target organs associated with body fluid homeostasis:

vascular smooth muscle, kidney, specific brain regions (OVLT, SFO), adrenal cortex, and pituitary

Clinically useful in lowering BP

Losartan is an Ang II receptor blocker: dec vasoconstriction, vasopressin release from post. pituitary, and aldosterone release

Atria are passively filled with blood returning from general circulation.

Greater blood volume stretches the atria - able to determine blood volume by amount of stretch

Baroreceptors on the venous and arterial side project to the NTS.

NTS neurons project to the parabrachial nucleus (PBN)

PBN neurons project to the SON and the PVN increasing the release of vasopressin.

Venous side of vasculature is very sensitive to changes in blood volume but causes small changes in VP release.

Arterial side of vasculature is less sensitive but causes greater changes in VP release.

Arterial baroreceptors innervate a large number of NTS neurons which allow for this greater response.

Both systems normally work together to maintain fluid balance.

If there are conflicting inputs, they must be prioritized by the system. Osmotic control overrides volemic mechanisms.

Barorecptors: synapse on most distal dedrites

Osmoreceptors: synapse near axon hillock and can inhibit any baroreceptor activation of vasopressin release

Both are independent of one another.

The satiety mechanism monitors corrective behavior.