Fluid and electrolyte homeostasis
Water balance
Sodium balance and extracellular fluid connection
Potassium balance
Behavioral mechanisms controlling salt and water
Integration control of volume and osmolarity
Acid-base balance examples
Homeostasis depends on:
Kidneys
Respiratory system
Cardiovascular system
Thirst and water craving are behavioral mechanisms linked to physiological needs via the hypothalamus.
The hypothalamus connects behavioral and physical aspects (e.g., stress and sickness, hunger and sugar needs).
Kidneys conserve water but cannot create it.
Decreased blood pressure and volume response:
Volume receptors in atria and carotid/aortic baroreceptors.
Sympathetic innervation increases heart rate and cardiac output.
Vasoconstriction increases blood pressure.
Hypothalamus contains osmoreceptors.
Low volume leads to high osmolarity, triggering ADH (Antidiuretic Hormone) formation.
ADH causes kidneys to conserve water.
Hypothalamus triggers thirst, increasing fluid intake and blood pressure.
Increased blood volume increases blood pressure.
Detected by beta receptors triggering parasympathetic response.
Reduced cardiac output and vasodilation lower blood pressure.
No ADH production leads to water excretion in urine, reducing volume and blood pressure.
Water balance is maintained by the urinary system, requiring external water intake.
High volume increases blood pressure and GFR, leading to more fluid in urine.
Low volume decreases GFR, conserving water until normal levels are reached.
Medulla of kidneys sets threshold for what exits the tubular system.
Higher osmolarity in the medulla concentrates urine.
Fluid in the descending loop of Henle loses water via osmosis.
Cells in the thick ascending limb are water-impermeable, transporting sodium out to reduce osmolarity.
Distal nephrons control water reabsorption via hormones like ADH.
Diuresis is excess water removal; diuretics promote urine excretion for high blood pressure or heart failure.
Membrane recycling allows vasopressin (ADH) to control water permeability in distal tubules and collecting ducts via aquaporins (water holes).
Nocturnal anuresis is bed wetting.
The medullary area has higher osmolarity.
Water reabsorption occurs due to osmotic/oncotic pressure.
Isotonicity or iso-osmolarity is maintained.
The ascending limb pumps ions (e.g., sodium) out without water.
The distal part of the tubule and collecting ducts reabsorb water under ADH control.
Vasopressin = vasoconstriction (increases blood pressure)
Antidiuretic hormone = prevents urination (increases volume and pressure)
Triggered by conditions that drop blood pressure or reduce water (e.g., dehydration).
Hypothalamic osmoreceptors sense these conditions.
Made in hypothalamus, released by posterior pituitary gland.
Works on renal collecting ducts & distal tubules for water reabsorption.
Ascending limb pumps sodium out, water follows, diluting the medulla.
Renal system uses a countercurrent exchange system.
Vasa recta (straight blood vessels) remove water from the medulla to prevent dilution.
Fluid in the descending loop of Henle loses water to the medulla.
As fluid ascends, sodium, potassium, and chloride are pumped out, reducing osmolarity.
Vasa recta takes up water to maintain osmolarity.
Responsible for sodium reabsorption; water follows.
Increases blood pressure.
Activates B cells of collecting ducts to reabsorb sodium, excreting potassium.
High aldosterone = increased sodium, decreased potassium.
Triggered by low blood pressure.
Stimulates adrenal cortex to produce aldosterone (a steroid).
Increases blood pressure.
Stimulates aldosterone synthesis.
Increases vasopressin release.
Increases thirst.
Indirect effect on the cardiovascular center (medulla oblongata).
Increases sympathetic innervation and cardiac output.
Vasoconstriction (primary function).
Sodium and hydrogen ion exchanger.
Angiotensin II Functions:
Vasoconstriction.
Activates cardiovascular center and induces sympathetic innervation.
Increases vasopressin release and thirst.
Stimulates adrenal cortex to produce aldosterone.
Increases sodium and water reabsorption.
Production and Activation:
Angiotensinogen (inactive) is made in the liver.
Renin (from juxtaglomerular cells in kidneys) activates angiotensinogen into angiotensin I in response to decreased GFR.
Angiotensin Converting Enzyme (ACE) converts angiotensin I into angiotensin II in the blood vessels (especially in the lungs).
ACE Inhibitors: block ACE to slow down the production of angiotensin II, treating high blood pressure.
Potassium, kalemia, cardiac.
Aldosterone reabsorbs sodium but excretes potassium.
Hyperkalemia: Too much potassium, kidney has to kick out the sodium - causes:
Kidney diseases
Diarrhea
Diuretics
Hypokalemia: Low potassium level - leads to:
Muscle weakness, failure of the respiratory muscle and heart.
Hyperkalemia can lead into cardiac arrhythmias.
Normal plasma pH: 7.38 - 7.42
Controlled by hydrogen ion concentration.
pH modulates enzyme functionality; abnormal pH affects protein structure and nervous system.
Acidosis: Neurons become less excitable; CNS depression.
Alkalosis: Hyper-excitability.
pH disturbances are associated with potassium disturbances.
Kidneys pump potassium and hydrogen oppositely.
Example: Hyperkalemia leads to losing hydrogen ion, or acid, which leads to metabolic alkalosis.
Diet (fatty acids, amino acids)
Breathing (carbon dioxide from metabolism)
Water (forms carbonic acid)
Production of lactic acid and ketoacidosis
Buffer system (bicarbonate in extracellular fluid)
Proteins, hemoglobin, phosphates in cells
Phosphate and ammonia in urine
Respiratory system (ventilation)
Renal system (excretion of hydrogen)
Hyperventilation: Washing off carbon dioxide, losing acid (respiratory alkalosis).
Buffers control moderate pH changes.
Cellular proteins, phosphate ions, hemoglobin, and bicarbonate balance pH.
Ventilation rapidly corrects 75% of disturbances but cannot maintain long-term.
Receptor-mediated endocytosis.
Directly excretes or reabsorbs hydrogen ions.
Indirectly changes the rate at which bicarb buffer is reabsorbed or excreted.
Fluid and electrolyte homeostasis are crucial for maintaining cellular function, nerve impulse transmission, and overall physiological balance.
Water balance involves the regulation of water intake and output to maintain optimal hydration levels.
Sodium balance is closely linked to extracellular fluid volume, influencing blood pressure and fluid distribution.
Potassium balance is essential for proper cardiac and muscle function, with imbalances potentially leading to life-threatening arrhythmias.
Behavioral mechanisms, such as thirst and salt cravings, play a vital role in maintaining fluid and electrolyte balance by encouraging intake when needed.
Integration control mechanisms, including hormones and neural pathways, coordinate fluid and electrolyte regulation to maintain homeostasis.
Acid-base balance is critical for enzyme function and overall metabolic processes; imbalances can have severe physiological consequences.
Homeostasis depends on:
Kidneys: Regulate water excretion and reabsorption.
Respiratory system: Influences water loss through breathing.
Cardiovascular system: Maintains blood pressure and fluid distribution.
Thirst and water craving are behavioral mechanisms linked to physiological needs via the hypothalamus.
The hypothalamus connects behavioral and physical aspects (e.g., stress and sickness, hunger and sugar needs), ensuring that hydration and electrolyte levels are maintained in response to various stimuli.
Kidneys conserve water but cannot create it, highlighting the importance of external water intake.
Decreased blood pressure and volume response:
Volume receptors in atria and carotid/aortic baroreceptors detect changes and initiate compensatory mechanisms.
Sympathetic innervation increases heart rate and cardiac output to raise blood pressure.
Vasoconstriction increases blood pressure by narrowing blood vessels.
Hypothalamus contains osmoreceptors that monitor blood osmolarity, triggering appropriate responses to maintain fluid balance.
Low volume leads to high osmolarity, triggering ADH (Antidiuretic Hormone) formation, which promotes water conservation by the kidneys.
ADH causes kidneys to conserve water by increasing water reabsorption in the collecting ducts.
Hypothalamus triggers thirst, increasing fluid intake and blood pressure, thus restoring normal fluid volume.
Increased blood volume increases blood pressure.
Detected by beta receptors triggering parasympathetic response, which helps to lower blood pressure.
Reduced cardiac output and vasodilation lower blood pressure, maintaining balance.
No ADH production leads to water excretion in urine, reducing volume and blood pressure, which can occur when the body is adequately hydrated or overhydrated.
Water balance is maintained by the urinary system, requiring external water intake to compensate for daily losses and bodily functions.
High volume increases blood pressure and GFR, leading to more fluid in urine as the kidneys filter excess fluid.
Low volume decreases GFR, conserving water until normal levels are reached, ensuring that the body retains necessary fluids.
Medulla of kidneys sets threshold for what exits the tubular system, determining the final concentration of urine.
Higher osmolarity in the medulla concentrates urine, allowing the kidneys to excrete waste with minimal water loss.
Fluid in the descending loop of Henle loses water via osmosis as it moves into the hyperosmotic medulla.
Cells in the thick ascending limb are water-impermeable, transporting sodium out to reduce osmolarity, creating a concentration gradient.
Distal nephrons control water reabsorption via hormones like ADH, fine-tuning urine concentration based on the body’s needs.
Diuresis is excess water removal; diuretics promote urine excretion for high blood pressure or heart failure by interfering with sodium and water reabsorption.
Membrane recycling allows vasopressin (ADH) to control water permeability in distal tubules and collecting ducts via aquaporins (water holes), adjusting water reabsorption based on hydration status.
Nocturnal anuresis is bed wetting, often due to inadequate ADH production or responsiveness.
The medullary area has higher osmolarity, facilitating water reabsorption.
Water reabsorption occurs due to osmotic/oncotic pressure, driving water from the tubules into the surrounding tissues.
Isotonicity or iso-osmolarity is maintained in the loop of Henle to optimize water and solute reabsorption.
The ascending limb pumps ions (e.g., sodium) out without water, contributing to the high osmolarity of the medulla.
The distal part of the tubule and collecting ducts reabsorb water under ADH control, allowing for precise regulation of urine concentration.
Vasopressin = vasoconstriction (increases blood pressure) by constricting blood vessels.
Antidiuretic hormone = prevents urination (increases volume and pressure) by promoting water reabsorption in the kidneys.
Triggered by conditions that drop blood pressure or reduce water (e.g., dehydration), ensuring the body conserves water when needed.
Hypothalamic osmoreceptors sense these conditions, initiating ADH release.
Made in hypothalamus, released by posterior pituitary gland, allowing for quick and coordinated response.
Works on renal collecting ducts & distal tubules for water reabsorption, increasing water retention.
Ascending limb pumps sodium out, water follows, diluting the medulla, which is essential for creating the concentration gradient.
Renal system uses a countercurrent exchange system in the loop of Henle to maximize water reabsorption.
Vasa recta (straight blood vessels) remove water from the medulla to prevent dilution, maintaining the high osmolarity needed for water reabsorption.
Fluid in the descending loop of Henle loses water to the medulla, concentrating the tubular fluid.
As fluid ascends, sodium, potassium, and chloride are pumped out, reducing osmolarity, which helps to create a dilute filtrate.
Vasa recta takes up water to maintain osmolarity, preventing the medulla from becoming too dilute.
Responsible for sodium reabsorption; water follows, increasing blood volume and maintaining electrolyte balance.
Increases blood pressure by increasing sodium and water retention.
Activates B cells of collecting ducts to reabsorb sodium, excreting potassium, regulating electrolyte balance.
High aldosterone = increased sodium, decreased potassium, affecting blood pressure and cardiac function.
Triggered by low blood pressure, initiating a cascade of hormonal responses to increase blood volume and pressure.
Stimulates adrenal cortex to produce aldosterone (a steroid), ensuring long-term regulation of sodium and potassium levels.
Increases blood pressure through multiple mechanisms.
Stimulates aldosterone synthesis, enhancing sodium and water reabsorption.
Increases vasopressin release, further promoting water retention.
Increases thirst, encouraging fluid intake to raise blood volume.
Indirect effect on the cardiovascular center (medulla oblongata), influencing sympathetic and parasympathetic activity.
Increases sympathetic innervation and cardiac output, raising blood pressure and maintaining perfusion.
Vasoconstriction (primary function), narrowing blood vessels to elevate blood pressure.
Sodium and hydrogen ion exchanger, regulating pH and electrolyte balance.
Angiotensin II Functions:
Vasoconstriction, increasing blood pressure.
Activates cardiovascular center and induces sympathetic innervation, enhancing cardiac output and blood pressure.
Increases vasopressin release and thirst, promoting fluid retention and intake.
Stimulates adrenal cortex to produce aldosterone, increasing sodium and water reabsorption.
Increases sodium and water reabsorption, expanding blood volume and maintaining electrolyte balance.
Production and Activation:
Angiotensinogen (inactive) is made in the liver and is the precursor to angiotensin II.
Renin (from juxtaglomerular cells in kidneys) activates angiotensinogen into angiotensin I in response to decreased GFR, initiating the RAAS cascade.
Angiotensin Converting Enzyme (ACE) converts angiotensin I into angiotensin II in the blood vessels (especially in the lungs), completing the activation process.
ACE Inhibitors: block ACE to slow down the production of angiotensin II, treating high blood pressure by reducing vasoconstriction and fluid retention.
Potassium, kalemia, cardiac: Potassium levels are critical for proper cardiac function, and imbalances can lead to arrhythmias.
Aldosterone reabsorbs sodium but excretes potassium, maintaining electrolyte balance.
Hyperkalemia: Too much potassium, kidney has to kick out the sodium - causes:
Kidney diseases: Impair potassium excretion.
Diarrhea: Loss of potassium-rich fluids.
Diuretics: Some diuretics increase potassium excretion.
Hypokalemia: Low potassium level - leads to:
Muscle weakness, failure of the respiratory muscle and heart, affecting overall bodily function.
Hyperkalemia can lead into cardiac arrhythmias, which can be life-threatening.
Normal plasma pH: 7.38 - 7.42, which is essential for optimal physiological function.
Controlled by hydrogen ion concentration, maintaining a narrow range for proper enzyme activity.
pH modulates enzyme functionality; abnormal pH affects protein structure and nervous system, disrupting bodily processes.
Acidosis: Neurons become less excitable; CNS depression, impairing brain function.
Alkalosis: Hyper-excitability, leading to muscle spasms and seizures.
pH disturbances are associated with potassium disturbances, as the body attempts to maintain electrical neutrality.
Kidneys pump potassium and hydrogen oppositely.
Example: Hyperkalemia leads to losing hydrogen ion, or acid, which leads to metabolic alkalosis, illustrating the interconnectedness of electrolyte balance.
Diet (fatty acids, amino acids) can affect pH through metabolic processes.
Breathing (carbon dioxide from metabolism) influences pH as carbon dioxide forms carbonic acid.
Water (forms carbonic acid) contributes to pH balance but can also lead to imbalances.
Production of lactic acid and ketoacidosis lowers pH, leading to acidosis.
Buffer system (bicarbonate in extracellular fluid) neutralizes excess acids or bases to maintain pH.
Proteins, hemoglobin, phosphates in cells act as buffers to minimize pH changes.
Phosphate and ammonia in urine help to excrete excess acids, maintaining pH levels.
Respiratory system (ventilation) controls carbon dioxide levels, affecting pH rapidly.
Renal system (excretion of hydrogen) regulates pH by excreting or reabsorbing hydrogen ions.
Hyperventilation: Washing off carbon dioxide, losing acid (respiratory alkalosis), increasing blood pH.
Buffers control moderate pH changes by neutralizing excess acids or bases.
Cellular proteins, phosphate ions, hemoglobin, and bicarbonate balance pH, maintaining homeostasis.
Ventilation rapidly corrects 75% of disturbances but cannot maintain long-term control.
Receptor-mediated endocytosis reclaims filtered proteins and other molecules.
Directly excretes or reabsorbs hydrogen ions, fine-tuning pH levels.
Indirectly changes the rate at which bicarb buffer is reabsorbed or excreted, regulating acid-base balance.