Szmigielska H, Szmigielski A, Szadowska A
Department of Pharmacodynamics Medical Academy, Lódź, Poland.
Pol J Pharmacol Pharm. 1989 Sep-Oct;41(5):413-9.
The responsiveness of the endogenous type II inhibitor of protein kinases to clonidine was used as an index of the reactivity of alpha 2-adrenoceptors in the brain. The stimulation of postsynaptic alpha 2-adrenoceptors by clonidine resulted in a dose-dependent decrease in type II inhibitor activity. In the nucleus tractus solitarii and anterior hypothalamus of spontaneously hypertensive rats (SHR) and renal hypertensive rats (RHR) the clonidine-induced decrease in type II inhibitor activity was markedly reduced. In contrast, clonidine was equipotent in reducing type II inhibitor activity in the hippocampus of those rats and in control normotensive animals. In addition to that, in SHR and RHR the hypothermic activity of clonidine was not reduced. Thus, it seems that in experimental hypertension the decrease of the reactivity of alpha 2-adrenoceptors occurs in the brain structures responsible for the blood pressure regulation.
蛋白激酶内源性II型抑制剂对可乐定的反应性被用作大脑中α2-肾上腺素能受体反应性的指标。可乐定对突触后α2-肾上腺素能受体的刺激导致II型抑制剂活性呈剂量依赖性降低。在自发性高血压大鼠（SHR）和肾性高血压大鼠（RHR）的孤束核和下丘脑前部，可乐定诱导的II型抑制剂活性降低明显减少。相比之下，可乐定在降低这些大鼠海马体和对照正常血压动物的II型抑制剂活性方面具有同等效力。此外，在SHR和RHR中，可乐定的降温活性并未降低。因此，在实验性高血压中，α2-肾上腺素能受体反应性的降低似乎发生在负责血压调节的脑结构中。
