Unknown

Dataset Information

0

Effects of 1 alpha,25-dihydroxycholecalciferol on sodium-ion translocation across chick intestinal brush-border membrane.


ABSTRACT: By utilizing isolated brush-border vesicles, Na+ transport across the luminal membrane of chick small intestine was found to be a composite of (i) a saturable (Km 10mM-Na+) amiloride-sensitive Na+/H+ antiport and (ii) a potential-sensitive conductive pathway. No evidence was obtained for the existence of a Na+/Cl- symport system. With the exception of the duodenum, luminal Na+ transfer in the entire small intestine was subject to regulation by vitamin D. Repletion of vitamin D-deficient chicks with 1 alpha,25-dihydroxycholecalciferol [1 alpha,25(OH)2D3] significantly decreased net Na+ uptake by isolated membrane vesicles (by approximately 30%). The sterol suppresses the conductive pathway (25-45% inhibition) as well as the Na+/H+ antiport system. Kinetic analysis of the latter revealed that 1 alpha,25(OH)2D3 altered Vmax (from 12.9 to 4.8 nmol of Na+/20s per mg of protein), but did not change Km. Diminution of Na+ transfer, entailing an increase in the electrochemical transmembrane Na+ gradient, provides an explanation of the simultaneously observed stimulatory action of 1 alpha,25(OH)2D3 on Na+-gradient-driven solute transport in chick small intestine. Indirect evidence was obtained that the luminal plasma membrane of chick small intestine displays a definite H+ permeability that is positively affected by 1 alpha,25(OH)2D3.

SUBMITTER: Fuchs R 

PROVIDER: S-EPMC1152635 | biostudies-other | 1985 Sep

REPOSITORIES: biostudies-other

Similar Datasets

| S-EPMC1186515 | biostudies-other
| S-EPMC1161516 | biostudies-other
| S-EPMC1162941 | biostudies-other
| S-EPMC1161252 | biostudies-other
| S-EPMC1161942 | biostudies-other
| S-EPMC3992856 | biostudies-literature
| S-EPMC1185817 | biostudies-other
| S-EPMC1201624 | biostudies-literature
| S-EPMC1153578 | biostudies-other
| S-EPMC1162681 | biostudies-other