Na-K ATPase (augmented by aldosterone or DCA), at basolateral aspects of enterocytes, pumps Na out of cell into interstitium, thus creating a lumen/cell electrochem. gradient for Na absorption from the GIT lumen, augmented by:
i) substrate dependent Na carriers which require either glucose, Cl, fructose, galactose, L-amino acids or peptides in lumen so that these are also absorbed into cell and passively diffuse down conc. gradient into interstitium;
ii) Na-H exchange at apical membrane of enterocyte which absorbs Na and secretes H into lumen. The H in lumen then may combine with luminal bicarb. to form CO2 which is lipid soluble and readily diffuses into enterocyte where carbonic anhydrase hydrates it to H2CO3 which then disassociates to bicarb. & H. ⇒ i/luminal bicarb. assists Na absorption;
iii) solvent drag accounts for a large % Na absorption in areas of bowel where tight jns are leaky such as jujenum; In these regions, interstitial Na may leak back on lumen but the water flow through the tight jns due to high interstitial [glucose] creates net Na absorption;
excretion:
Although some via sweat ([] 5-40mM), faeces ([] 10-90mM) these are not regulated - only renal is: <1% filtered Na is excreted in urine;
normal changes in GFR do not effect excretion unles severe depletion or incr. ECFV;
Fine regulation is probably at distal tubule where Na reabsorption is incr. by aldosterone;