SODIUM BALANCE AND REG OF CIRCULATING VOLUME Flashcards
(26 cards)
actual vs recommended dietary sodium intake
ACTUAL: 3,393 mg/day
RECOMMENDED: 2,300 mg/day
actual exceeds recommended
Main excretory pathway for Na+
in urine to match amount of ingested Na+ in the diet
Isosmotic water loss
occurs when there is no difference in osmolarity in the fluid leaving the ECF
- examples: in diarrhea
Fluid shift: water deprivation (volume contraction)
decrease in volume if both ECF and ICF, and INCREASE in osmolarity of in both ECF and ICF
Fluid shift: high NaCl intake (volume expansion)
decrease in ICF volume and increase in ECF volume, and increase in osmolarity in both compartments
Fluid shift: Infusion of isotonic NaCl
increase in volume of the ECF and no change in osmolarity of both compartments
Euvolemia
the steady state of Na+ reabsorption where [Na+] and ECF volume are normal and intake=excretion
What happens when there is an increase in Na+ intake?
there is a short period of time where Na+ intake exceeds Na+ excretion and the body holds onto water before intake and excretion become equal
- kidneys don’t work THAT fast, which is good not to overwhelm the system and be able to tolerate changes in homeostasis
Ions that compose most of the extracellular osmolarity
Na+, Cl- and HCO3-
Effective circulating volume
the volume of blood that effectively perfuses the body’s tissues
- unmeasurable volume that reflects the degree of filling in the arterial system
- depends on ECF volume, CO, plasma volume and MAP under normal conditions
- should otherwise be directly proportional to changes in ECF
Pathological example of ECV/ECF mismatch
in congestive heart failure
- heart doesn’t pump as well, which leads to decreases in CO and MAP, and ECF increases (buildup of blood since not circulating as much) but ECV decreases
filtered load
the amount of a substance (mg) that is filtered per minute
= GFR x Plasma concentration of substance
- for Na+, excreted Na+= filtered Na+ - reabsorbed Na+, which should be almost 0
glomerulartubular balance
describes the kidney’s ability to respond to changes in perfusion through the kidneys
–> increased GFR –> increased protein in the capillaries –> increased oncotic pressure –> increased reabsorption at PT
- an increase in filtrated Na+ and water is compensated with increased Na+ and water reabsorption to avoid severe Na+ and water depletion
- maintains constant ~2/3 reabsorption at the proximal tubule
when is RAAS activated?
excessive fluid loss in the body
- i.e hemorrhage= blood loss, diarrhea= water and electrolyte loss
- times of volume depletion
renal alpha 1 adrenergic receptors
innervate both afferent and efferent arterioles and increases renin secretion, while decreasing urinary sodium excretion and renal blood flow with SNS activity
- mostly present on Afferent arterioles
- SNS activity drives more sodium reabsorption
where is renin made?
juxtaglomerular cells of kidney
where is Angiotensin I cleaved into Angiotensin II?
lungs and kidneys, where they have ACE
Adrenal cortex role in RAAS activation
has receptors for Angiotensin II that promote aldosterone release–> incr Na+ reabsorption, increased NHE activity–> incr Na+ reabsorption, increased thirst& ADH secretion and vasoconstriction –> to incr TPR
Effect of Aldosterone on sodium reabsorption
acts on principal cells of the late DT and CD that have ENaC receptor and Na+/K+ pump to increase Na+ reabsorption
DIRECT effects of Angiotensin II on Na+ reabsorption
ATII stimulates Na+ reabsorption by increasing activity at the NHE transporter at PT
- besides direst stimulation of Na+ reabsorption, ATII also directly stimulates aldosterone production, vasoconstriction and decreased renal blood flow and excretion rate
what does ATII do to RBF?
DECREASES it!
- ATII constricts both afferent/efferent arterioles (prefers Efferent at low levels)
what does ATII do to GFR?
INCREASES/RESTORES IT
DIRECT effects of Angiotensin II on water reabsorption
receptors for ATII in the hypothalamus stimulate thirst and ADH secretion to increase water reabsorption
Hypervolemia
state of elevated blood volume or high MAP
