INCREASED SODIUM-DEPENDENT D-GLUCOSE TRANSPORT IN THE JEJUNAL BRUSH-BORDER MEMBRANE OF SPONTANEOUSLY HYPERTENSIVE RAT

Citation
Cm. Vazquez et al., INCREASED SODIUM-DEPENDENT D-GLUCOSE TRANSPORT IN THE JEJUNAL BRUSH-BORDER MEMBRANE OF SPONTANEOUSLY HYPERTENSIVE RAT, Pflugers Archiv, 432(2), 1996, pp. 329-335
Citations number
37
Categorie Soggetti
Physiology
Journal title
ISSN journal
00316768
Volume
432
Issue
2
Year of publication
1996
Pages
329 - 335
Database
ISI
SICI code
0031-6768(1996)432:2<329:ISDTIT>2.0.ZU;2-K
Abstract
The current studies explore the effect of hypertension on D-glucose tr ansport into jejunal brush-border membrane vesicles (BBMV). Spontaneou sly hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats, as a control group, were used. The purity of the BBMV from both groups of animals was validated by the finding that the specific activity of brush-border enzyme marker, sucrase, was severalfold greater in membr ane vesicles compared with corresponding values in mucosal homogenate. D-glucose uptake was Na+ dependent in both groups of animals, with a transient increase in the intravesicular concentration of D-glucose. H owever, the initial rate and the magnitude of the accumulation of Na+- dependent D-glucose was significantly higher in SHR compared with WKY rats. In order to investigate the mechanism(s) for the increase in Na-dependent D-glucose transport in SHR, several experiments were perfor med: (1) an experiment that indicated Na-22 uptake, as an indicator fo r Na+ permeability, was similar between SHR and WKY rats, (2) kinetic studies that indicated that V-max values of SHR were significantly gre ater that those of WKY rats. In contrast, similar K-m values for gluco se were found between SHR and WKY rats, (3) Na+-dependent phlorizin bi nding measurements that were not altered by hypertension and (4) a stu dy of the brush-border membrane lipid composition that showed a signif icant increase in the free cholesterol/phospholipid ratio in SHR. We c onclude that altered membrane cholesterol content and consequently alt ered lipid fluidity could be, at least in part, responsible for the ob served increase in Na+-dependent D-glucose transport in SHR.