We analyzed the contribution of soluble guanylate cyclase-dependent pathway into NO-mediated relaxation of pulmonary arteries under conditions of high pulmonary blood flow modeled by creation of carotid artery-jugular vein shunt in rats. Inhibitor of soluble guanylate cyclase suppressed NO-donor induced relaxation was lower in rats with shunt, but dilatation in response to phosphodiesterase V inhibitor did not differ in the sham-operated and shunt groups. Thus, the structure of NO-mediated vasodilatation of pulmonary arteries under conditions of hypervolemia of pulmonary circulation was shifted to soluble guanylate cyclase-independent pathways, whereas intracellular soluble guanylate cyclase-dependent mechanisms of dilatation were in general unchanged.

中文翻译：

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大鼠肺循环高血容量模型改变 NO 介导的肺动脉舒张结构

我们分析了可溶性鸟苷酸环化酶依赖性通路在高肺血流量条件下对 NO 介导的肺动脉舒张的贡献，该条件通过在大鼠中建立颈动脉-颈静脉分流来模拟。可溶性鸟苷酸环化酶抑制剂抑制 NO 供体诱导的舒张在分流大鼠中较低，但对磷酸二酯酶 V 抑制剂的反应在假手术组和分流组中没有差异。因此，在肺循环血容量过多的条件下，NO 介导的肺动脉血管舒张的结构转变为可溶性鸟苷酸环化酶非依赖性途径，而细胞内可溶性鸟苷酸环化酶依赖性扩张机制通常没有改变。