Physiological Regulatory Mechanisms: Ingestion, Water Balance, and Feeding
Physiological Regulatory Mechanisms
- Homeostasis: process by which the body’s substances and characteristics are maintained at their optimal level.
- System variable: variable controlled by a regulatory mechanism.
- Set point: optimal value of the system variable.
- Detector: signals when the system variable deviates from the set point.
- Correctional mechanism: mechanism capable of changing the value of the system variable.
- Negative feedback: the effect of an action serves to diminish or terminate that action.
- Thermostat analogy:
- Detector → Air temperature (system variable) → Heat (correctional mechanism) → Temperature setting (set point) → Negative feedback
- Electric heater (correctional mechanism)
Fluid Compartments and Balance
- Intracellular fluid (ICF): fluid inside cells.
- Extracellular fluid (ECF): fluids outside cells, includes:
- Interstitial fluid
- Intravascular fluid (blood plasma)
- Isotonic: equal osmotic pressure to the contents of a cell.
- Relative sizes of fluid compartments: ext{Intracellular} = 67 ext{ extpercent}, ext{ Interstitial} = 26 ext{ extpercent}, ext Intravascular} = 7 ext{ extpercent}, ext{CSF} < 1 ext{ extpercent}
Osmotic and Hypovolemic Thirst
- Two types of thirst:
- Osmometric (osmotic) thirst: due to increased osmotic pressure of interstitial fluid relative to intracellular fluid.
- Hypovolemic (volumetric) thirst: due to reduced intravascular (blood) volume.
- Osmoreceptors detect changes in solute concentration of interstitial fluid.
- Receptors for thirst are located in circumventricular organs near the third ventricle:
- OVLT (organum vasculosum of the lamina terminalis)
- SFO (subfornical organ)
- Circumventricular organs lack a typical blood–brain barrier.
- Stimuli and receptors:
- Osmotic thirst: detected by osmoreceptors in OVLT/SFO.
- Hypovolemic thirst: detected by receptors that sense blood volume and by angiotensin II signaling.
- Angiotensin II role in thirst and salt appetite; RAAS involvement with hypovolemia.
- Receptors for osmotic/hypovolemic signals:
- OVLT and SFO near the third ventricle.
- SFO contains neurons that detect circulating angiotensin II.
Hormonal Control of Water Balance
- Vasopressin (antidiuretic hormone, ADH):
- Released by posterior pituitary.
- Increases blood pressure via vasoconstriction; promotes water reabsorption in kidneys; concentrates urine.
- Helps compensate for decreased water volume.
- Also implicated in reproductive behaviors.
- Inhibited by alcohol.
Volumetric Thirst and RAAS
- Hypovolemia triggers compensatory mechanisms to restore blood volume.
- Renin: hormone secreted by kidneys that converts angiotensinogen to angiotensin II: ext{Renin} + ext{Angiotensinogen}
ightarrow ext{Angiotensin II} - Angiotensin II: constricts blood vessels, promotes sodium and water retention, and stimulates thirst and salt appetite.
- SFO contains neurons that detect circulating angiotensin II and stimulate drinking.
Osmotic vs Hypovolemic Thirst: Quick Comparison
- Stimulus:
- Osmotic: high solute concentration outside cells → water moves out of cells.
- Hypovolemic: low blood volume.
- Best relief:
- Osmotic: water only.
- Hypovolemic: water with solutes.
- Receptors:
- Osmotic: OVLT and SFO.
- Hypovolemic: receptors measuring blood pressure in veins and the SFO.
- Hormonal influences:
- Osmotic: vasopressin secretion; angiotensin II increases with certain stimuli.
- Hypovolemic: increased by angiotensin II.
Integration of Water Balance
- Overall integration at the Median Pre-optic Nucleus (MPON): OVLT, SFO and nucleus of the solitary tract connect to the MPON.
- Output from MPON drives drinking behavior.
Feeding and Energy Homeostasis: Short-Term Signals
- Feast or famine concept: need for fuel and building blocks; balance with availability, metabolism, body weight, and nutrition.
- Glucose, insulin, and glucagon:
- Most digested fuel enters bloodstream as glucose; brain primarily uses glucose.
- After a meal: liver converts excess glucose to glycogen; fat cells store energy as fat.
- During low glucose: liver glycogen → glucose.
- Insulin rises around meals and after meals; high insulin generally decreases appetite.
- Blood chemical control of eating: pancreatic hormones regulate glucose homeostasis.
- Glucoprivation: dramatic fall in cellular glucose availability.
- Lipoprivation: dramatic fall in fatty acids available to cells.
- Brain uses glucose; other cells use both glucose and fatty acids.
- Liver contains sensory neurons that detect decreases in glucose and signal the brain via the vagus nerve (cranial nerve X).
Nutrient Receptors and Long-Term Satiety
- Receptors for glucose and lipids are located in the liver and convey signals about gluco- and lipoprivation to the brain via the vagus nerve.
- Leptin: hormone from adipose tissue involved in long-term satiety; more fat → more leptin; low leptin increases hunger; leptin gene mutations can affect feeding.
Brain Control of Feeding: Hypothalamic Regulation
- Lateral hypothalamus (LH): regulates hunger; feeding tends to increase when LH is activated.
- Ventromedial hypothalamus (VMH): regulates satiety; activation reduces feeding.
- Arcuate nucleus contains:
- NPY/AgRP neurons: stimulate hunger.
- POMC/CART neurons: promote satiety.
- Other regions involved include the thalamus, cerebral cortex, and midbrain structures influencing metabolism and arousal.
- A balance of excitation and inhibition among feeding circuits governs eating behavior.
Feeding Circuits and the Arcuate Nucleus
- NPY neurons in the arcuate nucleus: when excited, promote hunger.
- CART neurons (and related POMC pathways): promote satiety when activated.
- Interactions between hunger and satiety systems determine feeding decisions.
Main Concepts
- Balance between inhibition and excitation governs eating and drinking.
- Interactions between brain and body tissues regulate feeding, thirst, and fluid balance.
- Multiple regulatory mechanisms coordinate short-term signals (gastric, hormonal, metabolic) with long-term signals (adiposity/ leptin) for energy and fluid homeostasis.