Mechanism of ammonium transport by intestinal segments following urinary diversion: evidence for ionized NH4+ transport via K(+)-pathways.

Using a previously reported in vivo intestinal perfusion model in the rat, we have shown that net total ammonium absorption accounts for the majority of the acid load resulting from urinary intestinal diversion. In the present study, by varying perfusate pH and therefore NH3 concentrations, we demonstrated that the net flux of total ammonium did not correlate with non-ionized NH3 concentrations (r = .039). This indicates that the basic mechanism of total ammonium flux is via ionized NH4+ movement. To more precisely define the transport processes involved, we manipulated this system with the following chemical and pharmacologic probes of electrolyte transport: amiloride (0.5 mM/l.), furosemide (1 mM/l.), 2,4,6-triaminopyrimidine (TAP) (15 mM/l.), methylprednisolone (3 mg./100 gm./B.W.) S.Q. x 3 days followed by perfusion, and barium (Ba2+) (15 mM/l.). Net solute flux was not significantly altered by the mucosal addition of amiloride or TAP. Methylprednisolone treated rats exhibited significantly diminished Na+ secretion (p less than .01) and increased Cl- absorption (p less than .05) without affecting net total ammonium flux providing evidence for the inducibility of Na+ conductance channels and against significant NH4+ movement via this pathway. The mucosal addition of furosemide resulted in significantly decreased net absorption of both total ammonium (p less than .001) and K+ (p less than .05). The addition of Ba2+ resulted in a three-fold reduction of ammonium absorption (p less than .001) and a greater than ten-fold reduction in K+ absorption (p less than .001). The observation of significant inhibition of ammonium absorption by furosemide and barium suggests that K+ transport pathways play a significant role in the intestinal transport of NH4+.