title: Developmental aspects of sodium-dependent transport processes of preimplantation rabbit embryos.
abstract: It is well established that the trophectoderm of the preimplantation rabbit blastocyst can actively transport solutes that, in turn, are believed to mediate the accumulation of blastocoelic fluid. Consequently, the rabbit blastocyst serves as an ideal model to investigate epithelial transport mechanisms during embryonic development. The trophectoderm is considered to be an electrically "tight" epithelium, as values for the transepithelial electrical resistance and potential difference are high for both day-6 and day-7 p.c. blastocysts. However, during development the trophectoderm displays marked changes in epithelial transport properties, particularly between day 6 and day 7 p.c. These changes (see Fig. 14.1) are characterized by (1) the loss of a Na+-dependent methionine transport mechanism, (2) the development of an amiloride-sensitive component to Na+ influx, (3) a decrease in ouabain-sensitive oxygen consumption with a concomitant increase in ouabain binding, and (4) the acquisition of a furosemide-sensitive NaCl cotransport system. During this period the rate of fluid accumulation doubles, resulting in a five-fold increase in blastocoele volume. We have also presented results showing that individual proteins of expanding blastocysts can be grouped with respect to their synthetic rates and that plasma membrane proteins can be uniquely characterized by their apical and basolateral domains. We suggest that the dramatic changes in epithelial transport mechanisms observed during preimplantation development of the rabbit blastocyst are a consequence of the changing developmental expression of trophectodermal membrane constituents. The blastocyst tissue is thus a useful model not only for understanding epithelial transport function in general, but also for understanding the physiological events associated with normal embryonic development.
authors.forename: D J
authors.initials: DJ
authors.lastname: Benos
authors.forename: J D
authors.initials: JD
authors.lastname: Biggers
authors.forename: R S
authors.initials: RS
authors.lastname: Balaban
authors.forename: J W
authors.initials: JW
authors.lastname: Mills
authors.forename: E W
authors.initials: EW
authors.lastname: Overström
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000596:Amino Acids / Q000378:metabolism; D000666:Amphotericin B / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D001755:Blastocyst / Q000378:metabolism*; D003994:Bucladesine / Q000494:pharmacology; D002712:Chlorides / Q000378:metabolism; D047108:Embryonic Development; D005314:Embryonic and Fetal Development; D004848:Epithelium / Q000378:metabolism; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D011247:Pregnancy; D014176:Protein Biosynthesis; D011817:Rabbits; D012964:Sodium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
chemical_list: D000596:Amino Acids; D002712:Chlorides; D010042:Ouabain; D003994:Bucladesine; D000584:Amiloride; D005665:Furosemide; D000666:Amphotericin B; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase