“…However, particularly in enterocytes of the upper small intestine, which are challenged continuously by high daily rates of Ca2+ absorption and are therefore exposed to high concentrations of CaP, the mechanisms involved in maintaining [Ca2+]i at a low level are not well defined. Transcellular active Ca2P transport is facilitated in the presence of the vitamin Ddependent Ca2P-binding protein calbindin-D9k, which is under the control of calcitriol (Schroder, Kaune, Schlumbohm, Breves & Harmeyer, 1993), and it has been proposed that calbindin-D9k could also function as a protective buffer against free Ca2P ions (Nemere & Norman, 1991). In a previous in vitro study with Ussing chambers using isolated, intact epithelia of the small intestine of pigs with calcitriol deficiency and with low non-physiological mucosal calbindin-D9k concentrations (Fox, Maunder, Randall & Care, 1985), a greater stimulation of net electrogenic ion transport rates by certain secretagogues such as theophylline and A23187 was demonstrated (Schroder, Kaune & Harmeyer, 1991).…”