Jastrzebski Z, Czyzewska-Szafran H, Goźlińska B, Remiszewska M, Mazurek A P
Department of Pharmacology, Drug Institute, Warsaw, Poland.
Neurosci Lett. 1995 Jan 23;184(2):94-6. doi: 10.1016/0304-3940(94)11177-k.
The effect of gamma-aminobutyric acid (GABA)A receptors and of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor blockade on clonidine hypotension was studied. The experiments were performed on spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. We found that the blockade of GABAA receptors line significantly (P < 0.01) reduced hypotensive responses to clonidine. Similarly, the NMDA receptor antagonist dizocilpine (MK-801) completely abolished the blood pressure lowering effect of clonidine. Our findings support the conclusion that clonidine hypotension is closely related to the functional state of both inhibitory GABAergic and excitatory glutamatergic systems.
研究了γ-氨基丁酸（GABA）A受体以及谷氨酸受体N-甲基-D-天冬氨酸（NMDA）亚型的阻断对可乐定所致低血压的影响。实验在自发性高血压大鼠（SHR）和血压正常的Wistar-Kyoto（WKY）大鼠身上进行。我们发现，阻断GABAA受体明显（P<0.01）降低了对可乐定的降压反应。同样，NMDA受体拮抗剂地佐环平（MK-801）完全消除了可乐定的降压作用。我们的研究结果支持以下结论：可乐定所致低血压与抑制性GABA能系统和兴奋性谷氨酸能系统的功能状态密切相关。
