Jan4 M2-Sodium Homeostasis Flashcards
what’s the cause for the variations in our U Na
changes in dietary Na intake
what senses body sodium
PRESSURE receptors in the vascular wall, the renal AA and the heart
pressure receptors (baroreceptors) activation leads to changes in what
RAAS, SS, ADH and ANPs
impact of SS activation on the kidney (2)
SS stimulates juxtaglomerular cells to secrete renin
NE stimulates Na reabso in the PCT
diuretics mainly for what 2 conditions
edema and hypertension
Na in the PCT: %, mechanisms (3) and regulatory factors (3)
65%. Na channels + Na-H exchange + NaK ATPase drives Na+glucose,a.a,PO4 cotransporters.
AT2, NE and GFR
Na in loop of Henle: %, mechanisms (3) and regulatory factor
No reabso in the DL. TAL: 25%. NaK ATPase (baso), Na-K-2Cl cotransporter, Na-H exchanger, paracellular (tight junctions). flow-dependent
Na in the DCT: %, mechanism and regulatory factor
5%. NaK ATPase (baso), Na-Cl cotransporter. flow-dependent
Na in the collecting tubules: %, mechanism and regulatory factors (2)
3%, Na channels. aldo and ANP
other ion coming in with Na in CCD (CT) and how
Cl- paracellularly bc cation needs its anion
what goes outside CT to compensate on Na entry and how
K through K channel
aldosterone: hormone type, exact mode of action and on what exact cell
steroid hormone, binds aldoR in the nucleus of principal cells (CCD). aldoR acts as TF. more Na and K channels are made
AT2 and NE exact mode of action on the tubule in volume depletion
enhance Na reabso in PCT by increasing the activity of the Na-H exchanger
feedback loop in the RAAS
aldosterone feeds back on renin and suppresses it (baroreceptor feedback)
aldo produced where exactly, stimulus for its release and what exact molecule stimulates it + exact site of action of aldo
hypovolemia and AT2. zona glomerulosa. acts on CCD (CT)
aldo makes Na reabso vary by how much
0 to 2%. no aldo. 2% filtered load is excreted. with aldo: 0% filtered load is excreted
adrenal layers + fct and which are in cortex/medulla
cortex: zona glomerulosa (salt), zona fasciculata (sugar), zona reticularis (sex)
medulla: panic (catecholamines)
3 mechanisms by which renin is stimulated in hypovolemia
SS activity, drop in arterial P (less stretch on AA), less NaCl delivery to the macula densa
why does Na = volume
it is the main extracellular ion
2 things doing the opposite of aldo on Na excretion (2 other factors)
ANP and BP
how ANP acts to increase Na excretion (3)
- acts on CT (CCD) to stop eNac channels and decrease Na reabso
- GFR (AA dilation and EA constriction)
- inhibits aldo release
how BP acts on increase Na excretion
pressure natriuresis
what’s the result if all ingested Na is not excreted
increase in ECF volume (interstitial and intravascular)
what happens to IV volume if give 1L saline and why
increases by 250 ml because Na can’t cross cells. extra Na to the body always in ECF. contributes to ECF volume
good strategy to control BP
lower dietary Na intake
euvolemic % Na reabso in the tubule
PCT: 65% TAL: 25% DCT: 5% CCD: 3% 1% excreted
main changes in tubular Na reabso in hypovolemia
- 80% abso in PCT (AT2 and NE enhance Na-H exchanger)
- 0% excreted
main changes in tubular Na reabso in hypervolemia
50% reabso PCT
12% reabso DCT
6% excreted
4 volume regulation systems
SS, RAAS, ANPs, ADH
SS effects on kidneys in very low BP (severe hemorrhage, severe hypovolemia, ..)
- constricts renal arterioles to drop GFR (overrides renal autoregulation (of GFR))
- activates renin (RAAS)
tubules reaction in severe drop in BP
increase Na reabsorption
