INCREASED BRUSH-BORDER MEMBRANE CALCIUM-TRANSPORT IN THE INTESTINE, BUT NOT THE KIDNEY TUBULE, OF SPONTANEOUSLY HYPERTENSIVE RATS

Since we and others have found a decrease in intestinal Ca2+ absorptio n and renal Ca2+ reabsorption in the mature spontaneously hypertensive rat (SHR) at the tissue and cell level, we asked whether the transpor t defect was located at the luminal or the basolateral side of the epi thelial cell. We studied intestinal and renal Ca2+ transport using iso lated epithelial brush-border membrane vesicles (BBMVs) in order to ex amine the luminal side of this transport. For technical reasons, the p reparation of intestinal BBMVs was performed using a centrifugation te chnique, but for renal BBMVs a precipitation method was used. The vesi cles obtained with these two different techniques had markedly differe nt aspects by electron microscopy analysis. However, no morphological difference was apparent between the two rat strains for BBMVs of eithe r preparation. SHR and normotensive control Wistar-Kyoto (WKY) rats we re studied at the age of 5 and between 12 and 14 weeks, receiving a no rmal Ca (1%) and P (0.46%) diet. In 5 week old SHR, duodenal BBMV Ca2 uptake kinetics were similar to that of WKY of same age. However, in 12 week old rats mean (+/- SD) V. of duodenal Ca2+ uptake was signific antly enhanced in SHR compared with WKY (0.59 +/- 0.21 v 0.38 +/- 0.09 nmol/mg protein and 10 s, P < .01), whereas K(m) was similar in the t wo strains. By contrast, no difference was found for V(max) or K(m) of Ca2+ uptake in renal BBMVs in 12 week old rats. In conclusion, Ca2+ u ptake was either enhanced (duodenum) or normal (kidney tubule) in the mature SHR, compared with the WKY of same age. Therefore, decreased tr ansepithelial Ca2+ transport in these epithelia is not due to a defect at the luminal side, but must be located beyond the apical membrane s tructure.