Hoefke W, Kobinger W, Walland A
Arzneimittelforschung. 1975 May;25(5):786-93.
2-(2,6-Dichlorphenylamino)-(clonidine, Catapresan, Catapres), 2-(2,6-diethylphenylamino- (St 91), 2-(2-chloro-6-methylphenylamino)-, 2-(2-chloro-4-methylphenylamino)-, 2-(2-methyl-5-fluorophenylamino) -and 2-(2-chloro-3-methyl-phenylamino)-2-imidazoline were investigated in various pharmacological tests. 1. All substances increased blood pressure in spinal rats and initially in intact cats and dogs and increased the total peripheral resistance in the latter. As these compounds also showed mydriasis in conscious rats it has been concluded that these effects are due to stimulation of peripheral alpha-adrenoceptors. 2. With the exception of St 91 the substances lowered blood pressure following i.v. injection, they decreased heart rate in cats and dogs and the cardiac output in the latter. These four compounds also decreased heart rate in vagotomised and atropinised rats. It was concluded that these effects were due to a decrease in sympathetic activity of the CNS. 3. In anaesthetised rats with beta-adrenoceptor blockade by toliprolol, a blood pressure increase was elicited by i.v. injection of angiotensin and the resulting bradycardia was recorded as a measure of vagal reflex activity. Clonidine and three derivatives which have shown hypotensive activity facilitated the vagal cardiodepressor reflex; St 91 was inactive in this respect. It has been concluded that decrease in central sympathetic tone and increase in central vagal activity are linked together in these compounds. 4. St 91 did not lower blood pressure and did not facilitate vagal reflex bradycardia after i.v. injection in dogs, but was active after intracisternal injection. It has been concluded, therefore, that this compound is able to act on structures in the CNS like clonidine but these effects usually do not occur after systemic administration because of its poor ability to penetrate the blood-brain barrier. 5. All derivatives decreased gastric acid secretion. 6. All substances increased blood glucose levels and were sedative; St 91 was the least effective compound in both respects pointing to a central mediation of these effects. 7. The results show that clonidine and the derivatives tested have the same reaction pattern. 8. The relationship between the CNS mediated cardiovascular depression and the peripheral alpha-adrenergic stimulating potency in conjunction with the lipoid solubility have been discussed.
对2-(2,6-二氯苯基氨基)-(可乐定,卡塔普雷桑,可乐宁)、2-(2,6-二乙基苯基氨基)-(St 91)、2-(2-氯-6-甲基苯基氨基)-、2-(2-氯-4-甲基苯基氨基)-、2-(2-甲基-5-氟苯基氨基)-以及2-(2-氯-3-甲基苯基氨基)-2-咪唑啉进行了各种药理学试验。1. 所有物质均可使脊髓大鼠的血压升高,最初也可使完整的猫和狗的血压升高,并使后者的总外周阻力增加。由于这些化合物在清醒大鼠中也表现出散瞳作用,因此得出结论,这些作用是由于外周α-肾上腺素能受体受到刺激所致。2. 除St 91外,这些物质静脉注射后可降低血压,使猫和狗的心率降低,并使后者的心输出量减少。这四种化合物还可使迷走神经切断和阿托品化的大鼠心率降低。得出结论,这些作用是由于中枢神经系统交感神经活性降低所致。3. 在经托利洛尔阻断β-肾上腺素能受体的麻醉大鼠中,静脉注射血管紧张素可引起血压升高,并记录由此产生的心动过缓作为迷走神经反射活性的指标。可乐定和三种已显示出降压活性的衍生物促进了迷走神经心抑制反射;St 91在这方面无活性。得出结论,这些化合物中中枢交感神经张力的降低和中枢迷走神经活性的增加是相互关联的。4. St 91静脉注射后在狗中不会降低血压,也不会促进迷走神经反射性心动过缓,但在脑池内注射后有活性。因此得出结论,该化合物能够像可乐定一样作用于中枢神经系统中的结构,但由于其穿透血脑屏障的能力较差,这些作用通常在全身给药后不会出现。5. 所有衍生物均可降低胃酸分泌。6. 所有物质均可使血糖水平升高且具有镇静作用;在这两方面,St 91是效果最差的化合物,表明这些作用是由中枢介导的。7. 结果表明,可乐定和所测试的衍生物具有相同的反应模式。8. 讨论了中枢神经系统介导的心血管抑制与外周α-肾上腺素能刺激效能以及类脂溶解度之间的关系。