Fan C C, Powell D W
Proc Natl Acad Sci U S A. 1983 Sep;80(17):5248-52. doi: 10.1073/pnas.80.17.5248.
The role of Ca2+ and calmodulin in regulating coupled NaCl transport has been investigated in membrane vesicles from rabbit ileal brush border. Uptake of 22Na+ and 36Cl- was determined by a rapid filtration technique in vesicles isolated with a sucrose density gradient ultracentrifugation method. Ca2+ on the inside of the vesicle inhibited Na+ uptake when Cl- was the anion and Cl- uptake when Na+ was the cation by approximately equal to 30%. Ca2+ on the outside had no effect. When gluconate was the anion or when choline was the cation, Na+ or Cl- uptake was reduced by only 9-12%. A similar inhibition of D-[3H]mannitol uptake (10-17%) suggests this was due to a nonspecific decrease in the membrane permeability. Other cations such as Ba2+ and Mg2+ had no effect, but La3+ inhibited Na+ and Cl- uptake to the same degree as Ca2+. Calmodulin (2 microM) in combination with Ca2+ (1 microM, free concentration) significantly inhibited Na+ uptake when Cl- was the anion by 21-32% and Cl- uptake when Na+ was the cation by 20-27%. This effect was completely reversed by 10 microM trifluoperazine. When gluconate was the anion or when choline was the cation, Na+ or Cl- uptake was unaffected by Ca2+/calmodulin and trifluoperazine. The Ki for Ca2+ inhibition of Cl- -coupled Na+ uptake was reduced from 200 microM to 0.2 microM by incubation with 20 microM calmodulin. The Ki for exogenously added calmodulin studied at 1 microM Ca2+ was 0.2 microM. The Ki for trifluoperazine inhibition of the Ca2+/calmodulin response was 3 microM. These results represent compelling evidence for intracellular Ca2+/calmodulin regulation of coupled NaCl transport across the intestinal microvillus membrane. The exact mechanism of this regulation remains to be delineated.
已在兔回肠刷状缘的膜囊泡中研究了Ca2+和钙调蛋白在调节耦合NaCl转运中的作用。采用蔗糖密度梯度超速离心法分离囊泡,通过快速过滤技术测定22Na+和36Cl-的摄取量。当Cl-为阴离子时,囊泡内部的Ca2+抑制Na+摄取;当Na+为阳离子时,抑制Cl-摄取,抑制率约为30%。囊泡外部的Ca2+无此作用。当葡萄糖酸盐为阴离子或胆碱为阳离子时,Na+或Cl-摄取仅减少9 - 12%。对D-[3H]甘露醇摄取的类似抑制作用(10 - 17%)表明,这是由于膜通透性的非特异性降低。其他阳离子如Ba2+和Mg2+无作用,但La3+对Na+和Cl-摄取的抑制程度与Ca2+相同。钙调蛋白(2 microM)与Ca2+(1 microM,游离浓度)联合使用时,当Cl-为阴离子时,显著抑制Na+摄取21 - 32%;当Na+为阳离子时,抑制Cl-摄取20 - 27%。这种作用可被10 microM三氟拉嗪完全逆转。当葡萄糖酸盐为阴离子或胆碱为阳离子时,Na+或Cl-摄取不受Ca2+/钙调蛋白和三氟拉嗪的影响。通过与20 microM钙调蛋白孵育,Ca2+对Cl-耦合Na+摄取的抑制作用的Ki从200 microM降至0.2 microM。在1 microM Ca2+条件下研究的外源添加钙调蛋白的Ki为0.2 microM。三氟拉嗪对Ca2+/钙调蛋白反应的抑制作用的Ki为3 microM。这些结果有力地证明了细胞内Ca2+/钙调蛋白对跨肠微绒毛膜的耦合NaCl转运的调节作用。这种调节的确切机制仍有待阐明。