Utilisateur
- needs input from renal, CV and RP system
CV:
- fast
- under neural control
Renal:
- slow
- under endocrine/neuroendocrine control
- most abundant molecule
- 70 kg male contains 42 L H2O (60%)
- 26L intracellular fluid
- 3L plasma
- 11L interstitial fluid
- most water lost in urine
- small amt in GI tract
- water lost must be replaced by GI absorption
- Vol depletion = bp drop
- tisssues cant get adequate O2
- measured in osmolarity
- kidney controls urine osmolarity by varying water and Na that is absorbed
Too much Water:
- urine very dilute
- low osmolarity
Not Enough Water:
- urine is concentrated
- high osmolarity
Interstitial OsM of Renal Cortex:
- 300 mOsM
Interstitial OsM of Renal Medulla:
- 1200 mOsM
1) antidiuretic hormone-controlled variable water reabsorption in final tubular segments
- 65% water reabsorption is obligatory in proximal tubule
2) secretion of ADH increases permeability of tubule cells to water
- osmotic gradient exists outside tubules for trnapsort of water by osmosis
3) ADH is produced in hypothalamus and stored in posterior pituitary
- release of substance signals distal tubule and collecting duct, creating reabsorption of water
4)
During water deficit = secretion of ADH increases
- increases water reabsorption
During excess of water = secretion of ADH decreases
- more water is excreted
- most potent stimulues
- present in hypothalamus
- activated at plasma osmolarity of >280 mOsM
- less potent stimulus
- sensed by atrial stretch receptors
- decreased stretch activated ADH release
- conserves water
- less potent stimulus
- sensed by aortic and carotid baroreceptors
- decreased pressure activates ADH release
-conerseves water
- aquaporins insert on tubule surface of collecting duct cells
aquaporin = membrane channel protein for water
- aldosterone is a mineralocorticoid secreted by adrenal cortex (triggered by ANG 2)
- helps reabsorb Na in distal tubules and collecting ducts
- also leads to K secretion
- acts on principle cells of distal convoluted tubule and collecting duct
- intitiates translation of new pumps to reabsorb Na and excrete K
activation:
- increase extracellular K (hyperkalemia)
- decrease extracellular Na (RAAS)
- decrease BP/BV
inhibition:
- increase ECF osmolarity
