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首页> 外文期刊>American Journal of Physiology >A theoretical model of nitric oxide transport in arterioles: frequency- vs. amplitude-dependent control of cGMP formation.
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A theoretical model of nitric oxide transport in arterioles: frequency- vs. amplitude-dependent control of cGMP formation.

机译：一氧化氮在小动脉中运输的理论模型：cGMP形成的频率-振幅依赖控制。

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Nitric oxide (NO) plays many important physiological roles, including the regulation of vascular smooth muscle tone. In response to hemodynamic or agonist stimuli, endothelial cells produce NO, which can diffuse to smooth muscle where it activates soluble guanylate cyclase (sGC), leading to cGMP formation and smooth muscle relaxation. The close proximity of red blood cells suggests, however, that a significant amount of NO released will be scavenged by blood, and thus the issue of bioavailability of endothelium-derived NO to smooth muscle has been investigated experimentally and theoretically. We formulated a mathematical model for NO transport in an arteriole to test the hypothesis that transient, burst-like NO production can facilitate efficient NO delivery to smooth muscle and reduce NO scavenging by blood. The model simulations predict that 1) the endothelium can maintain a physiologically significant amount of NO in smooth muscle despite the presence of NO scavengers such as hemoglobin and myoglobin; 2) under certain conditions, transient NO release presents a more efficient way for activating sGC and it can increase cGMP formation severalfold; and 3) frequency-rather than amplitude-dependent control of cGMP formation is possible. This suggests that it is the frequency of NO bursts and perhaps the frequency of Ca(2+) oscillations in endothelial cells that may limit cGMP formation and regulate vascular tone. The proposed hypothesis suggests a new functional role for Ca(2+) oscillations in endothelial cells. Further experimentation is needed to test whether and under what conditions in silico predictions occur in vivo.
机译：一氧化氮（NO）发挥许多重要的生理作用，包括调节血管平滑肌的张力。响应血液动力学或激动剂刺激，内​​皮细胞产生NO，NO扩散至平滑肌，在其中激活可溶性鸟苷酸环化酶（sGC），导致cGMP形成和平滑肌松弛。但是，由于红细胞非常接近，因此血液会清除大量释放的NO，因此已经通过实验和理论研究了源自内皮的NO对平滑肌的生物利用度问题。我们为小动脉中的NO传输建立了数学模型，以检验以下假设：瞬时的，突发性NO生成可以促进有效的NO传递至平滑肌，并减少NO对血液的清除。该模型模拟预测：1）尽管存在诸如血红蛋白和肌红蛋白之类的NO清除剂，内皮仍能在平滑肌中维持生理上显着的NO含量; 2）在一定条件下，NO的瞬时释放是激活sGC的更有效方法，它可以使cGMP的形成增加数倍。 3）可以根据频率而不是振幅来控制cGMP的形成。这表明内皮细胞中NO爆发的频率以及Ca（2+）振荡的频率可能会限制cGMP的形成并调节血管张力。提出的假设表明内皮细胞中Ca（2+）振荡的新功能作用。需要进一步的实验以测试体内模拟预测是否发生以及在什么条件下发生。

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