Sodium-dependent retention of prostaglandins in rat ileum.

An intestinal perfusion technique is reported to study the steady-state ileal mucosal retention of labeled prostaglandins E1, E2, and F2 alpha in rats. Ileal homogenates were analyzed for [3H]prostaglandin E1, [14C]prostaglandin E2, and [14C]prostaglandin F2 alpha after intestinal segments were perfused with Krebs improved Ringer buffers containing sodium or depleted from sodium and replaced with choline, and buffers containing 1 mM ouabain, 2 mM amiloride, or 50 nM tetrodotoxin. Prostaglandin ileal mucosal uptake was also studied after iv injection of tetrodotoxin (20 micrograms/kg body weight). Prostaglandin concentration-dependent transport studies support passive uptake mechanisms for prostaglandin E1 and E2. Physiological concentrations of sodium increased labeled prostaglandins E1, E2, and F2 alpha ileal mucosal uptake and decreased n-octanol-buffer partition coefficients. Unlike sodium, potassium showed no effect on labeled prostaglandin ileal transport. Ouabain, amiloride, and tetrodotoxin in the perfusates did not significantly alter prostaglandin mucosal uptake. However, injecting tetrodotoxin into rats caused a drastic increase of prostaglandin uptake through the ileal mucosa. Therefore, the role of sodium on labeled prostaglandin E1, E2, and F2 alpha ileal mucosal transport can be postulated to be controlled by either one or both of the following mechanisms: a pH-partition passive transport mechanism, and/or a sodium channel-dependent pathway whereby prostaglandin permeation possibly proceeds via a sodium-prostaglandin ion-pair mechanism which is controlled by a gating phenomenon.