Lopaschuk G D, Michalak M, Tsang H
J Biol Chem. 1987 Mar 15;262(8):3615-9.
Pantothenic acid transport was studied in the isolated perfused rat heart and isolated sheep cardiac sarcolemmal vesicles. In the perfused heart, pantothenic acid transport was significantly greater if hearts were perfused as working hearts rather than Langendorff hearts, but was unaffected by the perfusion substrates used (11 mM glucose or 1.2 mM palmitate). Uptake rates of pantothenic acid in working hearts are dependent on perfusate concentrations of pantothenic acid (a Vmax of 418 nmol/g dry weight/30 min and a Km for pantothenic acid of 10.7 mircoM were obtained). Reduction in perfusate Na+ concentration from 145 to 105 mM (the Na+ was replaced with 40 mM choline) resulted in a small but significant decrease in pantothenic acid uptake. At 145 mM Na+, addition of a mixture of amino acids, whose uptake is Na+-dependent, resulted in a significant decrease in pantothenic acid uptake by the heart (173 +/- 5 to 132 +/- 12 nmol/g dry weight). If an inward Na+ gradient in isolated, purified sarcolemmal vesicles, was imposed, a rapid uptake of pantothenic acid was observed. Uptake rates are markedly reduced if Na+ was replaced by equimolar concentrations of K+ or if external Na+ was reduced below 40 mM. In the presence of Na+, increasing pantothenic acid concentrations resulted in an increase in pantothenic acid uptake by the vesicles. Combined, these data demonstrate that pantothenic acid is transported across the myocardial sarcolemmal membrane by a Na+-dependent mechanism, which may be common to a number of small molecules.
在离体灌注大鼠心脏和离体绵羊心肌肌膜囊泡中研究了泛酸转运。在灌注心脏中,如果将心脏作为工作心脏而非Langendorff心脏进行灌注,泛酸转运显著增加,但不受所用灌注底物(11 mM葡萄糖或1.2 mM棕榈酸)的影响。工作心脏中泛酸的摄取率取决于灌注液中泛酸的浓度(获得的Vmax为418 nmol/g干重/30分钟,泛酸的Km为10.7 μM)。将灌注液中Na+浓度从145 mM降至105 mM(用40 mM胆碱替代Na+)导致泛酸摄取略有但显著下降。在145 mM Na+时,添加其摄取依赖于Na+的氨基酸混合物导致心脏对泛酸的摄取显著下降(从173±5降至132±12 nmol/g干重)。如果在分离、纯化的肌膜囊泡中施加内向Na+梯度,则可观察到泛酸的快速摄取。如果用等摩尔浓度的K+替代Na+或使细胞外Na+浓度降至40 mM以下,摄取率会显著降低。在有Na+存在的情况下,增加泛酸浓度会导致囊泡对泛酸的摄取增加。综合这些数据表明,泛酸通过一种依赖于Na+的机制跨心肌肌膜转运,这可能是许多小分子共有的机制。