Morel N M, Dodge A B, Patton W F, Herman I M, Hechtman H B, Shepro D
Department of Biology, Boston University, Massachusetts.
J Cell Physiol. 1989 Dec;141(3):653-9. doi: 10.1002/jcp.1041410325.
Endothelial cell (EC) motility may contribute to the regulation of microvascular perfusion and/or paracellular permeability. The experiments reported herein demonstrate that bovine pulmonary microvessel EC can reversibly deform a silicone substrate in response to agents known to contract and relax smooth muscle cells. Contracting pulmonary microvessel EC exerted a tension that created wrinkles in the underlying deformable substrate. Relaxation and loss of tension were revealed by the disappearance of these wrinkles without loss of cell adhesion to the substratum. Angiotensin II (Ang II) and bradykinin stimulated pulmonary microvessel EC to contract within 3 to 8 min in a Ca2+-dependent fashion. The peak of contraction at 10 to 20 min was followed by relaxation. Forskolin and sodium nitroprusside (SNP) initiated relaxation of the microvessel EC within 3 to 10 min respectively. Relaxed EC contracted following the addition of Ang II, also within 3 min. Dibutyryl cAMP, dibutyryl cGMP, and the photoactivated internalized "caged" cAMP and cGMP promoted EC relaxation in a manner similar to forskolin and SNP. Increases in the intracellular concentration of inositol triphosphate (IP3) with the photoactivated IP3 complex promoted EC contraction in 2 min with a peak at 7 min. The contraction was followed by relaxation, which occurred at 20-25 min. Neither bovine pulmonary artery nor retinal microvessel EC, used as controls, contracted under these experimental conditions. One could speculate that this unique contractile property of pulmonary microvessel EC as observed in vitro may play a regulatory role in vivo, in local perfusion and/or in intercellular gap regulation.
内皮细胞（EC）的运动性可能有助于调节微血管灌注和/或细胞旁通透性。本文报道的实验表明，牛肺微血管内皮细胞可响应已知能使平滑肌细胞收缩和舒张的因子而可逆地使硅酮底物变形。收缩的肺微血管内皮细胞施加了一种张力，在下面的可变形底物上产生皱纹。这些皱纹的消失表明张力松弛，但细胞与底物的粘附并未丧失。血管紧张素II（Ang II）和缓激肽以Ca2+依赖的方式刺激肺微血管内皮细胞在3至8分钟内收缩。10至20分钟时收缩达到峰值，随后松弛。福斯可林和硝普钠（SNP）分别在3至10分钟内使微血管内皮细胞开始松弛。加入Ang II后，松弛的内皮细胞也在3分钟内收缩。二丁酰环磷酸腺苷（dibutyryl cAMP）、二丁酰环磷酸鸟苷（dibutyryl cGMP）以及光激活内化的“笼化”cAMP和cGMP以类似于福斯可林和SNP的方式促进内皮细胞松弛。光激活的肌醇三磷酸（IP3）复合物使细胞内IP3浓度增加，在2分钟内促进内皮细胞收缩，7分钟时达到峰值。收缩后随之出现松弛，发生在20至25分钟。用作对照的牛肺动脉和视网膜微血管内皮细胞在这些实验条件下均未收缩。可以推测，体外观察到的肺微血管内皮细胞这种独特的收缩特性可能在体内局部灌注和/或细胞间隙调节中发挥调节作用。
