Psyc417 Thirst Salt

Questions

Notes

Drinking too much water at once can cause water intoxication, drinking too much alcohol can just cause you to die.

There are physiological and environmental things that impact salt and water levels.

Water balance is strictly regulated by the body.

There is osmotic thirst (change in cell volume) volumetric thirst is change in blood volume.

Most fluid in your body is intracellular fluid, 1/3 being extracellular fluid.

Ossoreceptors

Osmoreceptors are neurons that detect the solute concentration of extracellular fluid. These receptors shrink in size when they are dehydrated firing rate increases, and then you are thirsty and want to drink. These neurons are located in the circumventricular organs.

Circumventricular organs do not have the normal blood brain barrier

Organum vasculosum of the lamina terminalis (OVLT), subfornical organ (SFO), and area postrema are circumventricular orgasn

Osmorceptors in SFO and OVLT drive water drinking. Damages to OVLT result in adipsia.

Osmoreceptors cause thirst and increase the amount that you retain.

Supraoptic nucleus of the hypothalamus contains osmoreceptors that media the secrution of vasopressin (antidiuretic hormone) from the posterio pitutitary clan, which increases water retention by the kidneys.

There is a syndrome where people do not excrete water, this causes water retention and weight gain (not fat gain). There is the opposite disorder, diabetes inspidus, that don't release vasopressin and they pee a lot (20 L a day!)

Vasopressin

Vassopressin has 2 main goals. The first is to constrict blood vessels (V1 receptor) and to reabsorb water to the blood (V2 receptor).

Hypovolemia

This is caused by a loss of fluid or blood, loss of sodium, this doesn't change the osmotic equilibrium (concetration doesn't change).

It is sensed via baroreceptors (these are mechanoreceptors). They are found in the main artery, heart left atrium, and pulmonary vessels.

Renin-Angiotensis system

Renin is released when the sympathetic nervous system activated the renal nerve.

This activates when renin is released following hypovolemia. This is also a very stressful response which activates the sympathetic system. Then Angiotensinogen (which is released by the liver) is converted by renin to angiotensin I, which gets converted to angiotensin II, in the subfornical organ, it binds to some neurons and then causes the retention of sodium (caused by aldosterone), water (caused by vasopressin), increase blood pressure, salt appetite, and drinking.

The highest density of AT1 is found in the SFO, OVLT, and cortex.

Blood loss is called hemorrhage.

The renin system being too active causes high blood pressure. This is the system that is targeted to treat hypertension.

Brain and Kidney correlation

Neurons in the SFO excite neurons in the OVLT and the median preoptic nucleus that drive immediate drinking.

PVN is always involved in fight or flight response. PVN releases CRH as the initial reponses to stress. It also releases vasopressin.

Salt Balance

Our bodies aren't good at storing salt. In the kidney there are structures that

The adrenal gland releases glucocortcoids and mineralocortiocoids (of which the aldosterone is the main one). Without aldosterone, the kindeys do not retain salt.

In the kidneys, sodium is reabsorbed from the kidneys in the distal tubule and the collecting duct. it increases the activitiy of Na+/K+ pup mps: this secretes postassium and reabsorbed sodium. It also increases activity of the distal tubule, sodium chloride costranrpoter (NCC). In the collecting duct, it increase activitiy of the epithelial sodium channel(ENaCs).

Also the sweat glands in the skin will retain salt.

Hyponatremia (low sodium) reflects electrolyte imbalance. This causes fatigue, lethargy,genearl feeling of exhaustion, seizures, coma and death.

Cerebral salt wasting: a volume-depleted and sodium-wasting datae, caused by head trauma, infections, encephalitis, CNS surgery, and other injuries.

After exercising you will have an appetite for salt. Exercise causes both osmotic and volumetric thirst.

In rodents, salt appetite increases the intake of a concentrated (normally rejected) 3% NaCl solution. In humans, they prefer 0.9% NaCl solution.

Furosemide induces salt appetite.

With a PBN/LH lesion it makes it so animals cannot express salt appetite.

Salt and Hypertension

Blood pressure rises with small salt injection (having too little is bad as not enough). when you don't eat enough salt then you paradoxically don't want to eat more salt. People who are hypertensive will have a high blood pressure and their minimum normal blood pressure is low salt intake, but normal people can have a normal blood pressure from moderate-low to moderate blood intake.

Some people are genetically predisposed to salt sensitivity and salt-sensitive hypertension. People who have hypertension seem to have elevated renin-angiotensin-aldosterone system.

Diet induced obesity (DIO) is accompapnied with salt retention and hypertension because the sympathetic nerve is active when you have positive energy balance (it stimulates lipolgenesis and heat generation) it increases blood perssure and salt rentention.

White fat cells actually have the ability to create angiotensin.Renal denervation presents DIO associated hypertension.

Having a good control of your blood pressure reduces the risk of alzheimer's disease or other forms of dimension. People who even had high blood pressure, antihypertensive medicine decreases the risk of alzheimer's and dementia.