Intestinal calcium (Ca2+) transport was examined at the cellular level using duodenal enterocytes isolated from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Compartmental analysis of 45Ca2+ uptake was performed on enterocytes isolated from young (12- to 14-wk-old) and mature animals (24- to 26-wk-old) fed either normal (1%) or high (2%) calcium diets. Intracellular Ca2+ flux (J(c)) was reduced in SHR compared with WKY for both young (0.67 ± 0.05 vs. 1.08 ± 0.08 nmol Ca2+ · mg protein-1 · min-1 P < 0.01) and mature (0.39 ± 0.03 vs. 0.71 ± 0.05 nmol Ca2+ · mg protein-1 · min-1; P < 0.001) animals on a normal calcium diet. On a high-calcium diet, this strain difference of J(c) disappeared in the young rats (0.87 ± 0.09 vs. 1.06 ± 0.06 nmol Ca2+ · mg protein-1 · min-1, NS). In mature SHR, the high-calcium diet stimulated J(c), whereas it lowered it in mature WKY resulting in a similar flux for both strains (0.56 ± 0.05 vs. 0.49 ± 0.05 nmol Ca2+ · mg protein-1 · min-1, NS). Young SHR had a lower intracellular Ca2+ pool compared with WKY. This defect was corrected by a high-calcium diet. The membrane Ca2+ flux (J(m)) was lower in mature SHR than WKY fed a normal calcium diet (P < 0.02); J(m) increased to the control value (P < 0.05) in the SHR on a high-calcium diet. Diet-induced changes of plasma 1,25-(OH)2 vitamin D levels in the SHR did not parallel the observed changes of intestinal Ca2+ fluxes. Thus duodenal enterocytes from SHR appear to have an intrinsic alteration of Ca2+ transport that can be corrected in part by a higher calcium diet.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - Jan 1 1989|
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