Augustine S J, Tachikawa S, Lokhandwala M F, Buckley J P
Chest. 1983 Feb;83(2 Suppl):328-31.
Studies were undertaken to investigate the role of the CNS in withdrawal hypertension caused by abrupt cessation of long-term clonidine treatment. The studies were conducted on male wistar rats receiving clonidine, 100 micrograms/kg subcutaneously twice daily for seven days. Withdrawal hypertension occurred 16 to 18 hours following the last injection of clonidine. Pressor responses to posterior hypothalamic stimulation were significantly potentiated in the rats undergoing clonidine withdrawal, and the depressor response to a single injection of 10 micrograms of clonidine into the lateral cerebral ventricle was significantly attenuated in these animals. Studies on pithed rats demonstrated that destruction of the CNS eliminated the withdrawal hypertension. These data suggest that alpha-adrenoreceptors in the nucleus tractus solitarius play an important role in the normal maintenance of blood pressure, and a decrease in sensitivity of these receptors could result in the development of a hypertensive state.
开展了多项研究以探究中枢神经系统在长期可乐定治疗突然停药所致撤药高血压中所起的作用。研究对象为雄性Wistar大鼠,每日皮下注射两次可乐定,剂量为100微克/千克,持续七天。在最后一次注射可乐定后16至18小时出现撤药高血压。可乐定撤药大鼠对下丘脑后部刺激的升压反应显著增强,而向这些动物侧脑室单次注射10微克可乐定的降压反应则显著减弱。对脊髓切断大鼠的研究表明,中枢神经系统的破坏消除了撤药高血压。这些数据表明,孤束核中的α-肾上腺素能受体在血压的正常维持中起重要作用,这些受体敏感性的降低可能导致高血压状态的发展。