Using isolated duodenal cells from spontaneously hypertensive rats (SHR) and their normotensive controls, Wistar-Kyoto rats (WKY), we previously showed that cellular calcium flux was decreased in SHR and that increasing dietary calcium (from 1 to 2%) eliminated strain differences in Ca2+ fluxes. The present study was carried out to investigate the role of calbindin-D9K and calmodulin in the flux difference and dietary calcium effects. Calbindin-D9K and calmodulin were separated by sodium dodecyl sulfate (SDS) gel electrophoresis in duodenal protein extracts of SHR and WKY (12-14 and 24-26 wk old) fed either a 1 or 2% calcium diet and measured by a ligand blotting (45Ca) technique. Young SHR had a significantly lower calbindin-D9K (P < 0.001) than did WKY on either diet. Calmodulin was significantly lower in young SHR than in WKY (P < 0.002). There was no strain difference in calmodulin in older rats fed the normal calcium diet. Calbindin-D9K was significantly decreased by the high-calcium diet in both strains at both ages. There was a significant correlation between duodenal calbindin-D9K and plasma levels of calcitriol (r = +0.80, P < 0.001) in WKY but not in SHR. Calmodulin was significantly decreased by dietary calcium in mature WKY (4.8 ± 0.2 vs. 3.7 ± 0.4 μg/mg cell protein, P < 0.03), demonstrating a potential regulation by dietary calcium of this protein. Finally, there was a significant correlation between calbindin-D9K and calmodulin (r = 0.59, P < 0.001) in WKY but not in SHR. In conclusion, the study points to abnormal regulation of both duodenal calbindin-D9K by calcitriol and duodenal calmodulin by dietary calcium in SHR. These findings probably explain previous observation of a different modulation of calcium fluxes by a high-calcium diet in SHR compared with WKY.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Issue number||3 30-3|
|State||Published - 1991|
- Ligand blotting
- Spontaneously hypertensive rats
ASJC Scopus subject areas