- Fluid balance - Na Flashcards
fluid balance
- isomotic fluiding fluiding leaving proximal tubule becomes progressively more concentrated in the descenfing limb
- removal of solute through thick ascending limb creates hyposomtic fluid
- hormones control distal nephron permeability to water and solutes
- urine osmolarirty depends on reapsorbtion in the collecting duct
Na+ balance
kidneys control Na+ reabsorption to maintain ECF volume & blood pressure
Na+ balance 2
• Na+ and ECF anions (HCO3- + Cl-) contribute 90% of the ECF osmotic activity
• Under normal conditions, the ECF can “retain” enough water to maintain osmolarity at 300 mOsm/L
– Add more salt to ECFretain more water = 300 mOsm/L • IncreasesECFvolume(bloodvolume)&bloodpressure
– Lose salt from ECFlose water = 300 mOsm/L
• Decreases ECF volume (blood volume & blood pressure)
Sources of Na+ input & output
To maintain a constant salt load, salt intake must equal salt output
Na+ reabsorption
• Nearly all Na+ is reabsorbed from the filtrate
• It is reabsorbed along the length of the tubule and plays different roles at each sit
* Descending limb of loop of Henle is the only place Na+ is not reabsorbed
Hormonal control – Na+ reabsorption
8% of Na+ reabsorption is hormonally controlled
– Distal convoluted tubule & collecting duct
– Renin-angiotensin-aldosterone system (RAAS) • Reabsorbs Na+ (increases blood volume & pressure)
– Natriuretic peptides
• Inhibits Na+ reabsorption (decreases blood volume & pressure)
Response to decrease in Na+ load
decrease Na > dc. arterial pressure >
1. > grf > net filtration
2. increase aldosterone > inc. na reabsorption
both lead to
dec exrection of na+ and accompanying cl- and fluid
> inc. conservation of nacl and accompanying fluid
haemorrohage recap
The baroreceptor response causes the constriction of the afferent arteriole which dec. GFR
RAAS - aldosterone
Na+ reabsorption in the distal tubule & collecting duct is controlled by the hormone aldosterone
- ## aldorsterone promotes the insertion of additional Na+ channels & pumps in the tubular cell membrane
RAAS stimulation
RAAS is stimulated by cells of the juxtaglomerular apparatus
• RAAS begins with the secretion of renin by the granular cells
• Renin secretion is stimulated by:
1. dec. stretch of the granular cells (ie. dec. blood pressure in the afferent arteriole)
2. dec. NaCl in the distal tubule (detected by macula densa cells)
3. Baroreceptor reflex (sympathetic stimulation of granular cells)
renin
trigers release of aldosterone
RAAS
- Granular cells secrete renin
- Renin activates angiotensinogen into angiotensin I
– Angiotensinogen is a plasma protein (high concentrations but inactive) - In lungs: Angiotensin I converted into angiotensin II by angiotensin-converting enzyme (ACE)
- Angiotensin II triggers release of aldosterone (hormone) from adrenal cortex
- Aldosterone stimulates Na+ reabsorption from distal tubule and collecting duct
- Water follows Na+ into ECF to restore blood volume & pressure
Natriuretic peptides (NP)
• Stimulates Na+ & water excretion to lower blood volume & pressure
• Producedbycardiomyocytesinthe – Atria (atrial natriuretic peptide - ANP)
- normal physiology
– Ventricles (brain natriuretic peptide – BNP)
- heart failure
• NP release is triggered by stretch of the heart chamber (inc. blood volume & pressure)