ATP: The red blood cell link to NO and local control of the pulmonary circulation
ATP: The red blood cell link to NO and local control of the pulmonary circulation
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DOI：
10.1152/ajpheart.1996.271.6.h2717
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发表时间：
1996-12-01
影响因子：
4.8
通讯作者：
Lonigro, AJ
中科院分区：
文献类型：
--
作者：
Sprague, RS;Ellsworth, ML;Lonigro, AJ
最近，我们报道了兔肺中肺血管阻力（PVR）的一氧化氮（NO）活性的表达需要兔红细胞（RBC）。在这里，我们研究了这样的假设：红细胞通过响应机械变形释放 ATP 参与 PVR 的调节，进而引起血管 NO 合成。我们发现兔子和人类的红细胞（但狗的红细胞则不然）会因机械变形而释放 ATP。为了确定这种 ATP 对 NO 合成和 PVR 的贡献，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。在人类红细胞存在的情况下，N-G-硝基-L-精氨酸甲酯（100 μM）会产生与血管口径减小一致的压力-流量关系的变化。 N-G-硝基-L-精氨酸甲酯对狗红细胞灌注的肺没有影响。这些结果表明了兔子和人类中控制 PVR 的独特机制，即红细胞响应机械变形而释放 ATP，刺激 NO 合成，进而调节 PVR。
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, N-G-nitro-L-arginine methyl ester (100 mu M) produced a shift in the pressure-flow relationship consistent with a reduction in vascular caliber. N-G-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.