Timmermans P B, Mackay J C, Fluitman P H, van Zwieten P A
Pharmacology. 1979;19(6):294-300. doi: 10.1159/000137328.
The experimental compounds St-1913, St-1966 and St-1967 in which the bridging nitrogen atom, as found in clonidine, has been replaced by a methylene (--CH2--) function, an oxygen or a sulphur atom, respectively, have been investigated with respect to their acute hypotensive effects in anaesthetized cats. Attention was paid to a possible contribution of the central nervous system to the hypotensive action of the drugs by means of vertebral arterial infusions. Although less active than clonidine, St-1913 and St-1967 are centrally acting hypotensive drugs. Central alpha-adrenoceptors are presumably involved in a similar manner as in the mechanism of clonidine. The hypotensive potency of St-1966 was much lower compared to the aforementioned drugs. A central origin for its depressor effects could be established. However, central alpha-adrenoceptors probably do not participate. In spite of its structural similarity with clonidine the mechanism of action of St-1966 appears to be different.
实验性化合物St-1913、St-1966和St-1967中，可乐定结构中的桥连氮原子分别被亚甲基（--CH2--）官能团、氧原子或硫原子取代。研究了它们对麻醉猫的急性降压作用。通过椎动脉灌注法，关注中枢神经系统对药物降压作用可能产生的影响。尽管St-1913和St-1967的活性低于可乐定，但它们是中枢性降压药物。中枢α-肾上腺素能受体可能以与可乐定机制类似的方式参与其中。与上述药物相比，St-1966的降压效力要低得多。可以确定其降压作用源于中枢。然而，中枢α-肾上腺素能受体可能并不参与。尽管St-1966与可乐定结构相似，但其作用机制似乎有所不同。
