Regulatory aspects of oxalate secretion in enteric oxalate elimination.

Enteric excretion of oxalate was studied in rats with chronic renal failure (CRF) by measuring the magnitude and direction of oxalate fluxes in vitro across short-circuited preparations of distal colon in Ussing chambers. The net absorptive flux of oxalate that is characteristic of colonic tissues removed from control rats was significantly changed to a net secretory flux in CRF rats. Injecting CRF rats with a specific angiotensin II (AngII) receptor (AT1) antagonist, losartan, results in a reversal of the CRF-induced net secretory flux (-13.87+/-0.08 pmol x cm(-2) x h(-1)) to an absorptive flux (+7.32+/-3.68 pmol x cm(-2) x h(-1)) by normalizing the unidirectional fluxes of oxalate. Similarly, oxalate fluxes were normalized across CRF colonic tissues by acute, in vitro application of losartan to the serosal bathing solution. It was also possible to simulate the CRF-induced secretory flux of oxalate (Jsm) in vitro across colonic tissues removed from control rats. Serosal application of AngII at 10(-6), 10(-5), and 10(-4) M resulted in significant increases in the s-->m flux of oxalate (increasing deltaJsm = 4.06+/-1.2, 8.41+/-0.94, and 13.8+/-3.8 pmol x cm(-2) x h(-1), respectively). Taken together, these results suggest that CRF-induced oxalate secretion is at least partly mediated by AngII, which is consistent with previous findings of a twofold upregulation of AT1 receptors in CRF colonic mucosa.