Reg of Sodium Balance & Extracellular Fluid Volume (Rao) Flashcards
To know: 1. The importance of maintenance of constant extracellular fluid volume (ECFV). 2. How body sodium balance determines ECFV. 3. Daily balance between sodium intake and output. 4. Sodium reabsorption in different segments of nephron. 5. How sodium balance is different from water balance. 6. Different receptors of ECFV. 7. Kidney responses to change in ECFV.
ECFV =
ECFV = ECF Na+ / PNa
At constant PNa, ECFV = ECF Na
PNa =
Amount ECF Na / ECFV
Change in body weight over a short period indicates what?
Na+ balance change
Output of Na+ (%ages)
Renal 80-90%
GI 0.5-10%
Skin 0-20%
Location and amounts of renal Na+ reabsorption (3 locations & % of 25000 mEq/day))
Proximal Tubule: Isotonic ~64%
Loop of Henle: ~28%
Distal tubule and CD: ~7%
S3 gallop & vein distension meaning
ECFV expansion
Decreased plasma albumin effect
reduced plasma colloid pressure -> edema
Time for recovery of diuresis after water intake
1-2 hrs
Time for recovery from input of Na+
2-4 days
Receptors for ECFV (location, action, result)
Neural stretch receptors - large veins - signals pituitary -> AVP/ADH -> regulates renal Na+ excretion
Atrial stretch receptors - atria - parasympathetic in vagus - AVP secretion -> sympathetics to kidney. Also ANP
Arterial baroreceptors - arteries - signals to pituitary -> AVP
5 regulators of Na excretion by kidney
Changes in GFR Aldosterone Natriuretic hormone Renin-Angiotensin system Others (sympathetic nerves, prostaglandins)
Changes in GFR result on Na+ filtered load
Proportional to GFR
Small changes in GFR undetectible, marked change in Na+
Pressure natriuresis
BP up –> 3-5 fold increase in urine & Na+ excretion. Autoregulation doesn’t totally compensate
Arterial pressure increase:
Acute effect in isolated kidney
Chronic effect in intact system
Acute - 2-3 fold increase by 30-50 mmHg
Chronic - compensates until 100-110 mmHg
(clarify?)
Aldosterone
source, stimulated/inhibited by
mineralcorticoid from adrenal cortex
Release stim by K+, angiotensin
Release inhibited by Na+
Acts exclusively on DCT and CD to increase Na+ reabsorption
Aldosterone mechanism
upregulates genes for:
Apical membrane Na Chanel in DCT and CD
Luminal NaCl cotransporter (increase Na reabs)
NKA (increase Na abs, K sec)
Slow acting
Natriuretic peptide (ANP) (source, stimulated/inhibited by)
Source - cardiac atrial cells (to plasma)
Stim by PNa increased or atrial distention
Renal tubular segments, renal blood vessels
ANP actions
Tubule - inhibits Na reabsorption
Renal vessel - increases GFR and Na excretion
Adrenal cortex - inhibits aldosterone secretion
Renin-Angiotensin
source, stimulated/inhibited by
Source - JG cells
Stim - Decreased ECF volume, increased sympathetic firing, decreased renal art BP
Inhib - expansion of ECF volume
Renin-Angiotensin
actions, cascade, result
Renin activates alpha2-globulin ->
Angiotensin I (converted by ACE to)
Angiotensin II
Effects:
Adrenal cortex -> aldosterone
Na reabsorption in DCT and CD
Sympathetic nervous effect on Na reabsorption
lowers GFR, incrases proimal sodium reabsorption
Prostaglandins, bradykinin, dopamine effect on Na reabsorption
produced in kidney
diuresis and natriuresis
Oubain-like factor
produced in atrium
diuresis & natriuresis
Which takes precedence for regulation - hypovolemia or hyponatremia
hypovolemia causes a more rapid response
