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Drinking Physiological Regulatory Mechanisms
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turbobusa
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Drinking Physiological Regulatory Mechanisms - 01-11-2013, 10:49 AM

– By Lacrima_Mortis

DRINKING PHYSIOLOGICAL REGULATORY MECHANISMS – maintains the constancy of some internal characteristic of the organism in the face of external variability

It contains 4 essential features:

1. system variable – characteristic to be regulated, such as body temperature

2. set point – optimal value of the system variable (98.6F)

3. detector – monitors the value of the system variable (such as an internal thermometer)

4. correctional mechanism – restores the system variable to the set point (such as shivering when cold, sweating when hot)

negative feedback – process by which the effect produced by an action serves to diminish or terminate that action (such as thermostat turning on heater when room temperature falls below set point and then the thermostat turns the heater off when the desired room temperature is reached)

satiety mechanisms – monitor activity of correctional mechanism, not the system variable, stopping the activity in anticipation of the replenishment that will occur later (that’s why we stop drinking after a few glasses of water when dehydrated, even before the fluid has reached our cells)

4 MAJOR FLUID COMPARTMENTS:

1 intracellular: fluid portion of the cytoplasm of cells

3 extracellular:

intravascular fluid (blood plasma)

cerebrospinal fluid

interstitial fluid (“seawater” around our cells)

Fluid compartments are separated by semipermeable barriers:

1. walls of capillaries separate interstitial fluid from blood plasma

2. cell membranes separate interstitial fluid from intracellular fluid

Intracellular

volume of intracellular fluid controlled by the concentration of solutes (solid substances dissolved in a solution) in the interstitial fluid

1. normally interstitial fluid is isotonic (the same concentration of solutes) with the intracellular fluid – water doesn’t move in or out of cell
2. if interstitial fluid loses water and becomes hypertonic (more concentration of solutes), water will then diffuse out of the cells

3. if the interstitial fluid gains water and becomes hypotonic (less concentrated), water will diffuse into the cells

balance is good – both hypertonia and hypotonia can damage cells
hypertonia causes impairment in cellular chemical reactions and hypotonia can result in rupture of the cellular membrane (too full of water)

Blood plasma
volume of blood plasma important to regulate, as changes can affect the heart
if blood volume is too high, blood pressure rises
if blood volume is too low (hypovolemia), the heart doesn’t pump effectively, resulting in heart failure
Interstitial fluid
if intracellular and intravascular fluid levels are kept normal, interstitial remains OK
so volume isn’t an issue; however, “tonicity” (concentration of solutes) is it is the tonicity which determines if water moves into or out of the interstitial fluid

KIDNEYS
composed of a million functional units – nephrons, which take fluid from blood and carry it to the ureter, which connects to bladder
kidneys control the amount of water and sodium that the body excretes – this affects both the volume and tonicity of the extracellular fluid
Amount of sodium and water excreted controlled by two hormones:
1. aldosterone – controls sodium excretion; steroid hormone released by adrenal cortex; high levels cause sodium retention
2. vasopressin – controls excretion of water; peptide hormone released by posterior pituitary gland; high levels cause water retention

Vasopressin is produced in cell bodies of neurons in two nuclei of the hypothalamus:
1. supraoptic nucleus
2. paraventricular nucleus

vasopressin is then transported in vesicles through the axons to the terminal buttons in the posterior pituitary gland; once released they enter the blood supply:
diabetes – lack of vasopressin; causes frequent urination; treat with nasal spray vasopressin

OSMOMETRIC THIRST – stimulated by cellular dehydration
occurs when the tonicity of the interstitial fluid increases, which draws water out of the cells (think of water seeking to be balanced), cells then shrink in volume
“osmosis” – movement of water, through semipermeable membrane, from low solute concentration to high solute concentration

RECEPTORS FOR OSMOMETRIC THIRST:
osmoreceptors – neurons that respond to changes in the solute concentration of the interstitial fluid – start firing when water is drawn out of them due to hypertonicity; most likely located in the anteroventral tip of the third ventricle (AV3V); if activated, they send signals to neurons that control rate of vasopressin secretion

High levels of vasopressin cause kidneys to retain water, sweating causes loss of water through skin, which increases tonicity of interstitial fluid, which then draws water out of the capillaries and cells
We can lose water only from the cells, but not intravascular, by eating a salty meal:

1. salt is absorbed from the digestive tract into the blood

2. this makes the blood hypertonic (high concentration of salt)

3. this draws water into the cell from the interstitial fluid

4. the loss of water from the interstitial fluid makes it hypertonic

5. now water is drawn out of the cells

6. as blood plasma increases in volume, kidneys excrete more water and sodium

7. eventually, excess sodium is excreted, along with the water that was taken from the interstitial fluid and intercellular fluid

8. this results in an overall loss of water from the cells

9. however, blood plasma volume never decreased (it actually was higher temporarily)

VOLUMETRIC THIRST – occurs when the volume of the blood plasma (intravascular volume) decreases

We can lose blood volume without affecting the interstitial compartment by:
1. direct loss of blood – which causes thirst and salt appetite (lose sodium in blood)

RECEPTORS FOR VOLUMETRIC THIRST:

1. Renin-Angiotensin System

kidneys contain cells that detect decreases in blood flow to the kidneys – detect hypovolemia
when detected, these cells secrete an enzyme, renin, which enters blood and is involved in synthesis of hormone, angiotensin, which then converts to angiotensin II (AII)
AII has multiple effects:
1. stimulates adrenal cortex to secrete aldosterone
2. stimulates posterior pituitary gland to secrete vasopressin
3. increases blood pressure by causing muscles in small arteries to contract
4. behaviorally it initiates drinking and produces a salt appetite

so, a reduction in blood flow to the kidneys results in retention of water and sodium, helps to compensate for their loss by reducing size of blood vessels, and motivates the animal to seek and ingest water and salt
2. Baroreceptors
sensory receptors in the atria of the heart that detect stretch
stretch receptors detect loss of blood volume

FOOD-RELATED DRINKING – most drinking occurs in anticipation of actual need, during meals; appears to involve angiotensin
Why?
1. eating causes water to be diverted from the rest of the body into the stomach and small intestine, to be used for digestion
2. once food is absorbed, it increases the solute concentration of the blood plasma and thus induces an osmometric thirst

SALT APPETITE – primary stimulus is presence of aldosterone, whose secretion is under the control of angiotensin

NEURAL CONTROL OF THIRST

Circumventrical system

OVLT and AV3V – contains osmoreceptors that stimulate thirst and vasopressin secretion; also receive information from baroreceptors in the heart nucleus of the solitary tract – in medulla, receives sensory information from the internal organs and taste buds and sends efferent axons to many parts of the brain, including the AV3V area damage to AV3V area can cause diabetes and lack of thirst (excessive urination, so must force self to drink)
subfornical organ (SFO) – circumventricular organ whose AII receptors are the site where angiotensin acts to produce thirst; it has few neural inputs, as its job is to sense the presence of a hormone in the blood; it has many outputs to various parts of the brain:

1. endocrine – SFO axons project to neurons in the supraoptic and paraventricular nuclei that are responsible for production and secretion of the posterior pituitary hormone vasopressin

2. autonomic – axons project to cells of the paraventricular nucleus and other parts of the hypothalamus, which the send axons to brain stem nuclei which control the sympathetic and parasympathetic nervous system; this system controls angiontensin’s effect on blood pressure

3. behavioral – axons sent to median preoptic nucleus, an area which controls drinking and secretion of vasopressin

median preoptic nucleus – receives info from:

1. OVLT regarding osmoreceptors

2. SFO regarding angiotensin

3. baroreceptors via the nucleus of the solitary tract

Lateral Hypothalamus and Zona Incerta

lesions of the hypothalamus disrupt osmometric and volumetric thirst, but not meal-associated drinking lesions of the zona incerta disrupt hormonal stimulus for volumetric thirst, but not the neural ones that originate in the atrial baroreceptors
zona incerta sends axons to brain structures involved in movement – influences drinking behavior

NEURAL CONTROL OF SALT APPETITE
sodium deficiency causes hypovolemia, which produces angiotensin, which stimulates adrenal cortex to release aldosterone
aldosterone stimulates receptors in the medial nucleus of the amygdala – but not solely responsible for salt appetite
zona incerta receives info from medial amygdala and also plays role in salt appetite

MECHANISMS OF SATIETY
receptors in the mouth and throat influence the amount of water consumed, but primary effects come from receptors in the digestive system, particularly in the small intestine and liver receptors in the mouth do not play a role in salt satiety; the liver has receptors which contribute to the satiation of a salt appetite; also, a hormone secreted in the atria of the heart plays a role – it is released when there is a rise in blood volume (remember, baroreceptors sense decline in blood volume)




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