Blastocoel expansion in the preimplantation mouse embryo: role of extracellular sodium and chloride and possible apical routes of their entry.
Blastocoel expansion in the preimplantation mouse embryo: role of extracellular sodium and chloride and possible apical routes of their entry.
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DOI:
10.1016/0012-1606(89)90312-6
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发表时间:
1989-05
影响因子:
2.7
通讯作者:
F. Manejwala;E. Cragoe;R. Schultz
中科院分区:
文献类型:
--
作者:
F. Manejwala;E. Cragoe;R. Schultz
The trophectoderm of the mouse blastocyst is a fluid transporting epithelium that is responsible for generating a fluid-filled cavity called the blastocoel. Vectorial transport of ions from the medium into the blastocoel generates an osmotic gradient that drives fluid across this epithelium. We report here that substitution of Na+ or Cl−, but not K+, in the medium halves the rate of blastocoel expansion in the mouse blastocyst. Entrance of Na+ into the trophectoderm may involve several routes, since both blastocoel expansion and 22 Na+ uptake are decreased in the presence of the highly specific Na+ H+ exchanger inhibitor, 5-(N-ethyl-N-isopropyl) amiloride, and to a lesser extent with the amiloride-sensit Na+-channel blocker, benzamil. Uptake of 22 Na+ manifests saturation kinetics as a function of extracellular Na+ concentration, whereas uptake of 36 Cl− is linear. Furthermore, neither 4, 4-diisothiocyanostilbene-2, 2-disulfonic acid, which is an inhibitor of the Cl− HCO− 3 exchanger, nor 2-(3, 4-dichlorobenzyl)-5-nitrobenzoic acid, which is a Cl−-blocker, affect either blastocoel expansion or 36 Cl− uptake. These results suggest that Na+ entry into the mouse blastocyst is carrier-mediated and probably involves several routes that include the Na+ H+ exchanger and possibly the Na+-channel. Chloride entry, however, may not be carrier-mediated and may occur through a paracellular route, ie, between the trophectodermal cells.