The Physiological Regulation of Thirst and Fluid Intake

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The Physiological Regulation of Thirst and Fluid
Intake

• Michael J. McKinley
• Alan Kim Johnson

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Why thirst?

• Habitual
• Cultural
• Psychogenic
• Regulatory response
• Reductions in fluid content in bodily
  compartments, hypertonicity of extracellular
  fluid, increase in dipsogenic hormone
  concentration
• Maintains volume and composition of body fluids

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Key Terms

• Hypertonicity high concentration of solutes
• Osmoreceptor sensory receptor that aids in the
  regulation of osmotic pressure
• Hypovolemia decreased blood/plasma volume due
  to dehydration
• Circumventricular lie outside blood-brain
  barrier
• Dipsogenic hormone causes thirst
• Ex. Angiotensin (ANG) II

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Cerebral Mechanisms

• Hypertonicity, cellular dehydration, and
  osmoreceptor stimulation
• Hypovolemia and extracellular dehydration
• Angiotensin (ANG) II dipsogenic hormone
• Afferent neural inflow
• Other hormonal signals
• Relaxin
• Atrial natriuretic peptide (ANP)

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Osmoregulation Intracelluar Dehydration

• 1 2 dehydration ? 1st signal for thirst
• Actually 1 2 increase in osmotic pressure in
  plasma
• Results from increased concentration of solutes
  (i.e. NaCl or sucrose)
• Only water, not solutes, cross cell membrane
  (osmosis)
• Osmoreceptors cause neural cues that initiate
  thirst
• Hypothalamus

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• The anterior wall of the third ventricle (AV3V)
  was the more likely site for osmotic thirst
  regulation and ruled Na concentration as an
  initiating factor.

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Neural Mechanisms Osmotically Stimulated Thirst

• Median preoptic nucleus (MnPO) responds to both
  hormonal osmotic stimuli from OVLT SFO
• Hormones i.e. relaxin, ANG II
• Osmoregulatory thirst may be blocked by ANG
  antagonists in the MnPO.
• Ultimately i blood pressure
• MnPO neurons may be osmoreceptive or receive
  neural input from other receptive parts of the
  brain.
• AV3V (lamina terminalis) is the location where
  stimuli from circulation, such as increased
  solutes or hormones (i.e. ANG II, relaxin),
  initiate thirst.

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Thirst Extracellular Fluid Volume Deficits
(Hypovolemia)

• Causes hemorrhage, sodium loss, edema
• Endocrine, autonomic, sympathetic nervous
  systems all work to maintain critical blood flows
  ? redistribute blood and interstitial fluids
• Eventually deficits must be corrected ? sodium
  intake ? thirst
• All systems need CNS to receive info regarding
  blood condition and/or interstitial volumes for
  extracellular fluid regulation.
• Both hormonal and visceral afferent pathways.

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Angiotensin Thirst

• Renin ANG II highly effective thirst inducers
  in rats.
• ANG-induced thirst requires lamina terminalis to
  sense circulating peptides and to use info
  derived from the CNS.
• The systemic and renin-angiotensin systems are
  hypothesized to be functionally coupled in
  regards to maintenance of body fluid homeostasis.

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Thirst Hindbrain Actions

• Baroreceptors (arteries) volume receptors
  (atria) in the hindbrain (medulla oblongata)
  control BP blood volume
• Increases result in inhibition of
  osmolarity-deemed thirst
• Baroreceptors and volume receptors act as
  negative feedback pathway to prevent overdrinking
• Decreases result in stimulation of thirst through
  initiation in the medulla (then to hypothalamus)

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Other Humoral Influences on Thirst

• Relaxin stimulates thirst
• Stimulates vasopressin secretion and water
  drinking when administered centrally or
  systemically
• ANGII relaxin work together to stimulate thirst
  during pregnancy
• ANP inhibits thirst
• Released by cardiac myocytes with high
  extracellular fluid volume to inhibit thirst and
  vasopressin secretion
• Directed mainly against ANG-stimulated drinking
  via circumventricular organs in the lamina
  terminalis
• SFO key site for these hormones

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Conclusion

• Not just one factor influences thirst.
• Osmotic, ionic, hormonal, nervous signals all
  work together w/CNS to regulate
• Pathophysiological influences can create
  overactivity or insensitivity to fluid loss (i.e.
  elderly)
• Psychogenic polydipsia -causes water intoxication
• A better understanding of neural pathways may
  give insight into the regulation of thirst and
  the associated disorders.

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Sources

• McKinley, M.J., Johnson, A.K. (February 2004).
  The Physiological Regulation of Thirst and Fluid
  Intake. News in Physiological Sciences. Vol. 19.
  www.nips.org.
• www.wikipedia.org
• Notes by Dr. Steve Gehnrich