Water Homeostasis Flashcards
when renal free water balance is zero, serum sodium concentration is ?
NORMAL (136-145 mmol/L)
when renal free water balance is positive, serum sodium concentration is ?
LOW = HYPONATREMIA (<136 mmol/L)
when renal free water balance is negative, serum sodium concentration is ?
HIGH = HYPERNATREMIA
osmolarity - defined
number of solute particles per 1 L of solvent
osmolality - defined
number of solute particles in 1 kg of solvent
water balance - defined
*regulation of the osmolality of body fluids
*purpose of regulating water balance is to maintain constant osmolality in your cells and body fluids
*purpose is to prevent movement of water between fluid compartments
*regulated by regulating renal water excretion
renal water excretion is determined by
- amount of solute in urine
- osmolality of urine
urine water excretion = ? (equation)
urine solute excretion / osmolality of urine
regulation of the osmolality of body fluids - overview
osmoreceptors in the hypothalamus act as sensor → modulate antidiuretic hormone AND triggers thirst mechanisms
major factors that regulate H2O handling
PATHWAY:
1. osmoreceptors
2. ADH
3. aquaporin water channels
DRIVING FORCE = hyperosmolar medulla
pathway leading to increased water excretion
decreased serum osmolality detected by osmoreceptors → suppression of ADH → water excretion
pathway leading to water retention
increased serum osmolality detected by osmoreceptors → activation of ADH → insertion of aquaporin channels + hyperosmolar medulla → water reabsorption
ADH & aquaporin (AQP2) channels - overview
*ADH binds V2 receptors in the principal cells (in cortical collecting duct) → increased cAMP (Gs subunit) → insertion of AQP2 channels on apical membrane that are permeable only to water → increased water reabsorption
note - aquaretics (vaptans) block this V2 receptor (prevent ADH from binding V2 → excrete additional water)
medullary concentration gradient
*concentration difference of solutes (NaCl, urea) within the kidney’s medulla
*creating a progressively increasing osmotic pressure from the outer → inner layer of the medulla
*allows for the concentration of urine by facilitating water reabsorption from the collecting duct
mechanisms contributing to making the medullary interstitium hypertonic
-
reabsorption of NaCl without water
-occurs in thick ascending loop of Henle via active transport via NKCC
-no H2O absorption
-diluting segment -
urea entry into the inner medullary interstitium
-via passive diffusion at the collecting duct
-urea re-enters tubular fluid at the loop - vasa recta
reabsorption of NaCl without water → hypertonic medullary interstitium
-occurs in thick ascending loop of Henle via active transport via NKCC
-no H2O absorption
-diluting segment
urea entry into the inner medullary interstitium → hypertonic medullary interstitium
*when ADH is present, additional urea is reabsorbed into the medullary interstitium → increased medullary concentration gradient → promotes water reabsorption in the collecting duct
*via passive diffusion
*urea re-enters tubular fluid at the loop
vasa recta contributes to → hypertonic medullary interstitium
*vasa recta helps to maintain the concentration gradient
*counter current mechanism utilizes energy to develop an osmotic concentration gradient along the medullary interstitium
*the layout of the vasa recta around its own Loops of Henle and the counter current flow that allows for the maintenance of the osmotic gradient
diluting vs. concentrating urine
*if volume overloaded, kidneys dilute urine to excrete increased H2O in excess of solute to dump the excess volume
*if volume depleted, kidneys concentrate urine to excrete less H2O in relation to solute to conserve H2O
*this is achieved by not only the presence/absence of ADH but also through development/maintenance of the hypertonic medullary interstitium
ADH secretion is regulated by
- plasma osmolality
- arterial volume
note - plasma osmolality is the primary trigger (arterial volume only contributes if there are large changes > 15%)
plasma osmolality & regulation of ADH secretion
*increased plasma osmolality → sensed by osmoreceptors → release of ADH (from posterior pituitary) to maintain osmolality → increased free water reabsorption
*decreased plasma osmolality → suppressed ADH release → decreased free water reabsorption (increased water excretion)
arterial volume & regulation of ADH secretion
*decreased arterial volume → decreased arterial stretch → increased ADH → increased water reabsorption → increased blood volume
*increased arterial volume → increased arterial stretch → decreased ADH → decreased water reabsorption (increased water secretion)
what is the MAIN trigger for ADH secretion
increased plasma osmolality
impaired free water excretion in diabetes insipidus
*a condition characterized by inability to concentrate urine & conserve water
*central: ADH not produced (hypothalamic or pituitary issue)
*nephrogenic: kidneys do not respond to ADH
*result: HYPERNATREMIA (increased serum sodium due to lack of water to dilute it)
impaired water excretion in syndrome of inappropriate ADH secretion (SIADH)
*sustained increase in ADH secretion that is NOT due to changes in plasma osmolality or changes in arterial volume
*sustained increase in ADH → increased water reabsorption → HYPONATREMIA (due to increased water volume AND increased sodium excretion due to plasma volume expansion)
effects of decreased Na+ and water intake on kidneys (SIMPLE)
*kidneys should REABSORB SODIUM AND WATER (i.e. decreased excretion of sodium and water)
effects of increased Na+ and water intake on kidneys (SIMPLE)
*kidneys should EXCRETE MORE SODIUM AND WATER (i.e. decreased reabsorption of sodium and water)
