Sprague R S, Ellsworth M L, Stephenson A H, Lonigro A J
Department of Medicine, Saint Louis University School of Medicine, Missouri 63104, USA.
Am J Physiol. 1996 Dec;271(6 Pt 2):H2717-22. doi: 10.1152/ajpheart.1996.271.6.H2717.
Recently, we reported that rabbit red blood cells (RBCs) were required for the expression of nitric oxide (NO) activity on pulmonary vascular resistance (PVR) in rabbit lungs. Here, we investigate the hypothesis that RBCs participate in the regulation of PVR via release of ATP in response to mechanical deformation that, in turn, evokes vascular NO synthesis. We found that rabbit and human RBCs, but not dog RBCs, release ATP in response to mechanical deformation. To determine the contribution of this ATP to NO synthesis and PVR, we compared the effects of human and dog RBCs on pressure-flow relationships in isolated rabbit lungs. In the presence of human RBCs, NG-nitro-L-arginine methyl ester (100 microM) produced a shift in the pressure-flow relationship consistent with a reduction in vascular caliber. NG-nitro-L-arginine methyl ester had no effect in lungs perfused with dog RBCs. These results suggest a unique mechanism for the control of PVR in rabbits and humans whereby release of ATP by RBCs in response to mechanical deformation leads to stimulation of NO synthesis that, in turn, modulates the PVR.
最近，我们报道兔肺中一氧化氮（NO）活性对肺血管阻力（PVR）的表达需要兔红细胞（RBC）。在此，我们研究了一个假说，即红细胞通过响应机械变形释放ATP来参与肺血管阻力的调节，而这种机械变形又会引发血管NO的合成。我们发现兔和人的红细胞，但不是狗的红细胞，会响应机械变形释放ATP。为了确定这种ATP对NO合成和肺血管阻力的作用，我们比较了人和狗的红细胞对离体兔肺压力-流量关系的影响。在存在人红细胞的情况下，NG-硝基-L-精氨酸甲酯（100微摩尔）使压力-流量关系发生偏移，这与血管管径减小一致。NG-硝基-L-精氨酸甲酯对灌注狗红细胞的肺没有影响。这些结果提示了兔和人控制肺血管阻力的一种独特机制，即红细胞响应机械变形释放ATP，进而刺激NO合成，反过来调节肺血管阻力。
