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autonomic final > lecture 17 (thrist) > Flashcards

lecture 17 (thrist) Flashcards

1
Q

what are the types of thirst

A

2 types
osmometric thirst: hypertonic interstitial fluid (high salt meal)
volumetric thirst: low blood volume (hemorrhage)

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2
Q

what are the body fluid compartments

A
  • intracellular compartments
  • extracellular
  • intravascular (in BV) /interstitial (not in vascular system)
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3
Q

describe what happens when you consume high salt meal (ie osmometric thirst)

A
  • high salt meal > blood plasma = hypertonic > hypertonic intravascular fluid causes osmosis out of interstitial fluid to normalize > now interstitial fluid becomes hypertonic > water is pulled out of intracellular compartment > sensed by osmoreceptors in OVLT/PVN/SON (VP releasing areas)
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4
Q

describe how osmoreceptors work

A

osmoreceptors expresses stretch-inhibited ion ch (stretched > closing of ch)
- hypertonic condition cause shrinkage of osmosensitive cells > increases opening of ion ch > depolarization (increase firing rate)
- hypotonic > stretch of membrane > decrease opening ion ch > inhibit depol (less firing rate)

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5
Q

where are osmoreceptors located and why is this specialized?

A

Located in OVLT PVN SON
But is specialized cuz OVLT = circumventricular organ with fenestrated capillaries allow for detection of tonicity of the blood

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6
Q

what are magnocellular neurons

A
  • cell bodies in hypothalamus PVN/SON
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7
Q

how does osmoreceptors correct hypertonic condition directly

A
  • 2 mecs:
  • increased release of VP (osmosensitive SON/OVLT neurons activated > project to SON/PVN to increase VP release)
  • activation of neural circuits that mediate thirst (OVLT neurons also project through median preoptic nuc MPN - thirst center)
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8
Q

describe indirect mechanism for release of VP

A
  • inhibitory interneurons monitor the size of OVLT osmoreceptors project to SON/PVN
  • IN extend dendrites around osmoreceptors and acts as mechanoreceptors = IN decrease firing as os R shrink (due to hypertonicity of interstitial fl)
  • with normal osmoreceptor cell volume (not shrink): interneuron inhibits VP release
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9
Q

describe “set point” for VP release? As a result…?

A

plasm os maintained within narrow limits > under a certain threshold, VP not released
- above the point VP is released in a linear fashion in relation of plasm os
- plasma [VP] increases before thirst is felt: meaning VP neurons more sensitive to os R output from OVLT than MPN

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10
Q

describe exception to the linearity VP release

A
  • rapid changes of plasm os > exaggerated VP release higher than predicted by linear
  • decrease VP while drinking (we can drink way faster than water can be absorbs into the system and signals to brain so decrease VP > prevent overdrinking )
  • during gestation os threshold for VP release is lowered
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11
Q

what are the different inputs that elicits volumetric thirst

A
  • baroreceptors in carotid sinus
  • atrial baro R in heart and large BV
  • JG cells in kidneys
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12
Q

how does baroreceptors in carotid sinus signal volumetric thirst

A

baro R decreases FR with decreased BV (decrease BP) > these receptors project to NTS > NTS sends projection to SON/PVN > increases release of VP > causing reabsorption water in kidneys
- ALSO NTS sends projections to MPN > elicits thirst

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13
Q

how does atrial baro R signal volumetric thirst

A

same way as carotid sinus baro R but less responsive > requires large change in pressure > induce large increase in VP + innervates large number of NTS > HUGE magnitude of response (experimentally confirmed in dogs)

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14
Q

how does JG cells signal volumetric thirst

A
  • kidneys monitor blood flow (decrease BF indicates decrease BV) > decrease flow causes JG cells to release renin into BS ?????
  • JG cells located near glomerulus and activates and release renin in response to drop in BP/decrease plasma sodium levels (direct)
  • JG cells receive inputs from SNS
  • expresses b adrenergic R (binding of NE > renin release) (indirect)
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15
Q

what does renin do

A
  • renin is protease (enzyme) > cleaves angiotensinogen > angiotensin 1 (dont do much) > cleaved again > angiotensin 2 (active)
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16
Q

describe the angiotensinogen pathway

A

angiotensinogen is prohormone always found in blood > renin is released (rate limiting) > cleaves angiotensinogen and forms angiotensin 1 (not active) > in lungs angiotensin converting enzyme (ACE) chops 1 to form 2

17
Q

what happens when theres conflicting input from os vs vol

A

conflicting input to neurons of SON and PVN (ie hyponatremia and low BV): osmotic control overrides volemic mechanisms (other mechanisms can support blood volume)

18
Q

how does body choose baro vs osmo

A

while both baro R and os R both project to SON/PVN, different receptors form synapses on different part of the target neuron
- baro R input synapse on most distal dendrits
- os R input synapse near axon hillock = closer to axon hillock = greater effect on if an action potential will fire
(can inhibit any baroreceptor act. of VP release)

19
Q

describe over night deprive water experiment

A
  • people are deprived of water overnight = exhibit both osmotic + volemic thirst > in the morning either IV water or IV isotonic saline
  • if IV injection water > osmosis out of vasculature and into dehydrated cells can take up the water > no osmotic thirst but volumetric thirst remains
  • individuals in this group experience significantly less thirst than water deprived control (85% less water)
  • if IV inject isotonic saline > replenishing the volume but not osmos into cells > still have osmos thirst but not vol thirst
  • these individuals drank (25% less water than control)
  • osmotic thirst more powerful
20
Q

how do we know when we’re no longer thirsty?

A
  • satiety mechanism for thirst is independent of detection of dehydration
  • amount of water consumed depends on input from several peripheral sources ie oropharynx/digestive
  • prevents overdrinking
21
Q

describe the ang 2 receptors

A

GPCR
AT1 R (most effects on fluid balance are mediated by AT1 R) expressed in SFO/OVLT, pituitary, vascular SM. kidney
- couples to Gq > stim PLC
AT2 R important during development

22
Q

ang 2 binds at AT1 R to mediate

A

Vasopressin release
Water drinking
Sodium retention
Sodium appetite
Vasoconstriction
ACTH release

23
Q

what is ang 2 how does it signal to brain

A
  • dipsogen (increase thirst measured by drinking behavior in animals)
  • too large to cross BBB
  • binds to R in SFO > SFO neurons projects (increase firing rate) to MPN and SON/PVN
24
Q

how is ang 2 important to the homeostasis of Na

A
  • volumetric thirst requires replenishment of water and sodium
  • Volumetric thirst occurs with loss of blood volume without a change in the osmolarity of the blood
  • if only water is replenished then the osmolarity of blood would decrease
  • Angiotensin II causes retention of sodium as
    well as water with volumetric thirst

autonomic final (8 decks)

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