The nature of choleresis induced by deoxycholate and its conjugates in the rabbit.

A hypothesis for the mechanism of bile salt-induced choleresis with increased bile bicarbonate concentration (cholehepatic recycling; CHR), requires a relatively high pK'a value of a bile salt to be easily protonated in bile canaliculi. If the choleresis induced by taurodeoxycholate and glycodeoxycholate (which increase bile bicarbonate concentration in rabbits) is to be explained by this thesis, these bile salts must be extensively deconjugated in the liver, enabling a bile salt having a higher pK'a value, free deoxycholate, to undergo CHR. With a stepwise increase in the infusion rate, the increments of bicarbonate concentration, as well as the bile flow rate induced by taurodeoxycholate and glycodeoxycholate, were as efficient as those caused by an equimolar infusion of deoxycholate. With infusion of conjugated deoxycholates, the major bile salts excreted in the bile were those which had been infused. In studies with conjugated deoxycholates, unconjugated deoxycholate was not detectable in the bile. Furthermore, deoxycholate concentration in the liver significantly increased after a 2-h infusion of deoxycholate but did not increase after infusion of either glycodeoxycholate or taurodeoxycholate. The present results suggest that the choleresis induced by conjugated deoxycholates in rabbits requires an explanation other than CHR of deoxycholate.