Rowe W A, Tomicic T K, Hajjar J J
Department of Medicine, Veterans Administration Medical Center, Newington, Connecticut 06111.
Proc Soc Exp Biol Med. 1991 Nov;198(2):754-9. doi: 10.3181/00379727-198-43315.
Vanadate alters intestinal transport and may have a role in regulating cell function. To determine whether it influences calcium absorption, we tested the effects of acute and chronic vanadate administration on calcium absorption using single-pass perfusion of jejunal and ileal segments of the in vivo rat intestine. Acute vanadate administration increased the lumen-to-mucosa and net fluxes of calcium in both the jejunum and ileum. The increase was largely due to an enhancement of the saturable fluxes of calcium and was observed at 10(-4) M concentration of vanadate, but not at higher or lower concentrations of the oxyanion, except at the highest concentration used, 10(-2) M, where calcium absorption was inhibited. Chronic vanadate administration caused, on the other hand, no changes in calcium absorption. We have demonstrated previously that rat intestinal (Na+ + K+)-ATPase is inhibited by vanadate, an effect that could raise cell sodium and increase the efflux of sodium across the brush border membrane. The results suggest that the vanadate enhancement of calcium absorption may be related to an increased entry of calcium into the mucosa, possibly as a result of an augmented exchange through the Na+/Ca+ antiport system. Alternatively, vanadate may influence access to a calcium channel in the mucosal membrane of the intestinal epithelium, leading to the observed increase in absorption.
钒酸盐可改变肠道转运,可能在调节细胞功能方面发挥作用。为了确定其是否影响钙吸收,我们利用体内大鼠肠道空肠和回肠段的单通道灌注,测试了急性和慢性给予钒酸盐对钙吸收的影响。急性给予钒酸盐增加了空肠和回肠中钙从肠腔到黏膜的通量以及净通量。这种增加主要归因于钙饱和通量的增强,在钒酸盐浓度为10⁻⁴ M时观察到,但在该含氧阴离子的更高或更低浓度下未观察到,除了所用的最高浓度10⁻² M,此时钙吸收受到抑制。另一方面,慢性给予钒酸盐对钙吸收没有影响。我们之前已经证明,大鼠肠道(Na⁺ + K⁺)-ATP酶受钒酸盐抑制,这种作用可能会提高细胞内钠含量,并增加钠通过刷状缘膜的外流。结果表明,钒酸盐对钙吸收的增强作用可能与钙进入黏膜的增加有关,这可能是通过Na⁺/Ca²⁺反向转运系统增强交换的结果。或者,钒酸盐可能影响肠道上皮黏膜膜中钙通道的可及性,从而导致观察到的吸收增加。