气道平滑肌兴奋-收缩耦合机制:药物设计的新靶点。

Drug design and delivery Pub Date : 1990-03-01
I W Rodger
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引用次数: 0

摘要

对气道平滑肌细胞内Ca2+水平的稳态调节以及细胞内Ca2+水平变化的后果进行了综述,并确定了一些机制作为药物作用的靶点。在预防哮喘方面——通过防止收缩的诱导——机会与受体拮抗、抑制Ca2+内流、抑制细胞内Ca2+释放、钙调素拮抗和收缩蛋白拮抗有关。在哮喘的症状缓解中——通过逆转既定的收缩反应——机会与Ca2+内流的抑制、肌醇三磷酸代谢的抑制、蛋白激酶C的抑制和Ca2+去除机制的增强有关。
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Excitation-contraction coupling mechanisms in airway smooth muscle: new targets in drug design.

Homeostatic regulation of Ca2+ levels within airway smooth muscle cells, and the consequences of changes in intracellular Ca2+ levels are reviewed, and a number of mechanisms are identified as targets for drug action. In the prophylaxis of asthma--by preventing the induction of contraction--the opportunities relate to receptor antagonism, the inhibition of Ca2+ influx, the inhibition of intracellular Ca2+ release, calmodulin antagonism, and the antagonism of contractile proteins. In the symptomatic relief of asthma--by reversal of established contractile responses--the opportunities relate to the inhibition of Ca2+ influx, the inhibition of inositol trisphosphate metabolism, the inhibition of protein kinase C, and the augmentation of Ca2+ removal mechanisms.

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