Kukovetz W R, Holzmann S
Z Kardiol. 1986;75 Suppl 3:8-11.
Nitrovasodilators relax vascular smooth muscle by one common mechanism, the activation of soluble guanylate cyclase leading to increased formation of cGMP. The considerable differences in potency between various nitrovasodilators appear, at least in part, to be due to the different pathways of their transformation into activators of guanylate cyclase such as nitrous oxide or nitrosothiol. Major differences were also found in the ability of these compounds to induce tolerance in isolated bovine coronary artery strips. Although the mechanism of tolerance development is still not clarified, it appears likely that cysteine deficiency may be responsible for this phenomenon since this thiol appears to be required for the transformation of certain nitrovasodilators (e.g. nitroglycerin) into stimulators of guanylate cyclase and also in the final step of activation of this enzyme.
硝基血管扩张剂通过一种常见机制使血管平滑肌松弛，即激活可溶性鸟苷酸环化酶，导致环磷酸鸟苷（cGMP）生成增加。各种硝基血管扩张剂在效力上的显著差异，至少部分原因是它们转化为鸟苷酸环化酶激活剂（如一氧化氮或亚硝基硫醇）的途径不同。在这些化合物诱导离体牛冠状动脉条产生耐受性的能力方面也发现了主要差异。尽管耐受性产生的机制仍未阐明，但半胱氨酸缺乏似乎可能是导致这种现象的原因，因为这种硫醇似乎是某些硝基血管扩张剂（如硝酸甘油）转化为鸟苷酸环化酶刺激剂所必需的，也是该酶激活的最后一步所必需的。
