Chapter 21 — Fluid and Electrolyte Balance

Drinking in response to thirst.

Cardiovascular reflexes that adjust heart rate, stroke volume, and arteriolar resistance.

The kidneys adjust sodium and water excretion under hormonal control.

Drinking fluids, water in food, and metabolic water produced during cellular respiration.

Urine, sweat, evaporation from the skin, water vapor in exhaled air, and feces.

The concentration of osmotically active particles in a solution.

Approximately 300 mOsm/L.

It can reach approximately 1200 mOsm/L.

Reabsorb water from the collecting ducts and produce concentrated urine.

The ascending limb reabsorbs salts but is essentially impermeable to water, so solute leaves without water following.

Primarily in the distal tubule and collecting duct.

Vasopressin, also called antidiuretic hormone (ADH).

Membrane channel proteins that allow water to cross cell membranes.

It causes aquaporin-2 channels to be inserted into the apical membrane of collecting duct cells, increasing water reabsorption.

More water is reabsorbed, producing a smaller volume of more concentrated urine.

Less water is reabsorbed, producing a larger volume of more dilute urine.

Vasopressin secretion generally increases during sleep, promoting water reabsorption and reducing urine production.

Osmoreceptors, baroreceptors, and volume receptors.

In the hypothalamus; they detect changes in extracellular fluid osmolarity.

In areas such as the carotid sinus and aortic arch; they detect arterial pressure and stretch.

In areas including the atria and large veins; they detect changes in blood volume and venous filling.

The posterior pituitary gland; it is synthesized in the hypothalamus.

Around 280–285 mOsm/L; the precise threshold varies.

Increased urine production.

Reduced urine production due to increased water reabsorption.

The loop of Henle and vasa recta work together to establish and preserve an osmotic gradient in the renal medulla.

It is permeable to water, so water leaves the tubule as the surrounding medulla becomes more concentrated.

It reabsorbs NaCl but is not permeable to water, making tubular fluid more dilute and increasing medullary osmolarity.

It acts as a countercurrent exchanger that carries away reabsorbed water and solutes while helping preserve the medullary osmotic gradient.

Salt increases extracellular osmolarity, stimulating thirst and vasopressin release so water intake and reabsorption increase.

An abnormally low concentration of sodium in the blood.

When water gain or retention is excessive relative to sodium, diluting the sodium concentration in plasma.

Aldosterone.

The adrenal cortex.

It increases sodium reabsorption and potassium secretion, especially in the distal nephron.

Angiotensin II and elevated plasma potassium.

Low plasma potassium and reduced stimulation by angiotensin II.

A hormonal pathway that helps defend blood pressure and blood volume by producing angiotensin II.

Low blood pressure or renal perfusion, sympathetic stimulation, and low NaCl delivery detected by the macula densa.

The liver.

Granular or juxtaglomerular cells in the kidney.

It converts angiotensinogen into angiotensin I.

Primarily on vascular endothelial surfaces, especially in the pulmonary circulation.

It converts angiotensin I into angiotensin II.

It causes vasoconstriction, stimulates aldosterone release, stimulates vasopressin release, increases thirst, and increases sympathetic activity.

It causes vasoconstriction, increasing peripheral resistance and blood pressure.

It stimulates aldosterone secretion, increasing renal sodium reabsorption.

It stimulates thirst, increasing water intake.

It promotes vasopressin release, increasing renal water reabsorption.

Natriuretic peptides, especially atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP).

Stretch of the heart caused by increased blood volume and pressure.

Increased sodium excretion in urine.

They promote sodium and water loss, reducing blood volume and blood pressure.

The kidneys, adrenal cortex, hypothalamus, and cardiovascular system.

They increase sodium and water excretion.

They inhibit aldosterone secretion, reducing sodium reabsorption.

They inhibit the renin-angiotensin pathway, reducing sodium retention and vasoconstriction.

They reduce vasopressin release and suppress thirst, decreasing water retention and intake.

They promote vasodilation, lowering peripheral resistance and blood pressure.

An abnormally low potassium concentration in the blood.

Muscle weakness, cramps, abnormal heart rhythms, and impaired cellular function.

An abnormally high potassium concentration in the blood.

Dangerous changes in cardiac electrical activity and potentially fatal arrhythmias.

Thirst and increased water intake.

Salt appetite, which increases sodium intake.

Isosmotic volume change, hyperosmotic volume change, and hypo-osmotic volume change.

Loss of water and solute in roughly equal proportions, reducing extracellular fluid volume without substantially changing osmolarity.

Loss of isotonic fluid, such as through severe diarrhea or blood loss.

Loss of proportionally more water than solute, increasing extracellular osmolarity.

Inadequate water intake or excessive water loss, such as heavy sweating without sufficient replacement.

Hypertonic dehydration can be especially challenging because increased osmolarity draws water out of cells.

Thirst increases water intake; vasopressin increases renal water reabsorption; the renin-angiotensin-aldosterone system promotes sodium and water retention; and cardiovascular reflexes defend blood pressure.

A measure of hydrogen ion concentration, defined as the negative logarithm of hydrogen ion concentration.

Approximately 7.35–7.45, with a typical value near 7.4.

Changes in pH alter protein charge and shape, which can change enzyme activity and protein function.

Carbon dioxide from metabolism, metabolic acids such as lactic acid and ketoacids, and acids produced during protein and phospholipid metabolism.

The lungs provide rapid regulation by controlling CO₂; the kidneys provide slower, sustained regulation by controlling hydrogen ion and bicarbonate handling. The lecture emphasizes ventilation as rapid and renal mechanisms as slow rather than assigning a fixed percentage.

They change ventilation to alter carbon dioxide levels, shifting the carbonic acid-bicarbonate equilibrium.

They secrete hydrogen ions, reabsorb filtered bicarbonate, generate new bicarbonate, and excrete acid in urine.

They secrete H⁺ into the tubule, excrete H⁺ buffered by phosphate, excrete ammonium, excrete titratable acids, and excrete other acid equivalents in urine.

They reabsorb filtered bicarbonate and generate new bicarbonate while excreting hydrogen ions.

Specialized cells in the collecting duct that regulate acid-base balance by secreting hydrogen ions or bicarbonate.

They secrete H⁺ into the tubular fluid and return bicarbonate to the blood, helping correct acidosis.

They secrete bicarbonate into the tubular fluid and retain hydrogen ions, helping correct alkalosis.

A condition in which blood pH is below the normal range.

A condition in which blood pH is above the normal range.

A decrease in pH caused by elevated CO₂, usually from inadequate ventilation.

An increase in pH caused by reduced CO₂, usually from excessive ventilation.

A decrease in pH caused by reduced bicarbonate or increased metabolic acid.

An increase in pH caused by increased bicarbonate or loss of hydrogen ions.

CO₂ increases, increasing hydrogen ion concentration and lowering pH.

CO₂ decreases, lowering hydrogen ion concentration and raising pH.

Bicarbonate decreases.

Bicarbonate increases.

A respiratory or renal response that moves pH toward normal without necessarily correcting the original cause.