Almazov V A, Zhdanova O N, Merkulova N K, Sitnikova M Iu, Shliakhto E V
Farmakol Toksikol. 1982 Sep-Oct;45(5):62-6.
A total of 178 patients with labile arterial hypertension were examined for the effect of propranolol and clonidine on the central hemodynamics, plasma renin, dopamine- beta-hydroxylase, urine kallikrein, and blood prekallikrein and kallikrein. The results suggest that basic to changes in the hemodynamics produced by a single administration of propranolol is its beta-adrenoblocking effect proper. The decrease in the general peripheral resistance due to prolonged propranolol therapy may be determined by activation of the blood kallikrein-kinin system and enhancement of the descending inhibition of the sympathetic nervous system because of activation of the central alpha-adrenoreceptors under long-term blockade of beta-adrenoreceptors of the central nervous system. The changes in the hemodynamics produced by low doses of clonidine may be accounted for by its central alpha-adrenomimetic effect.
对178例不稳定型动脉高血压患者进行了检查，以研究普萘洛尔和可乐定对中心血流动力学、血浆肾素、多巴胺-β-羟化酶、尿激肽释放酶以及血液前激肽释放酶和激肽释放酶的影响。结果表明，单次给予普萘洛尔所产生的血流动力学变化，其根本原因在于其本身的β-肾上腺素能阻断作用。长期使用普萘洛尔治疗导致总外周阻力降低，可能是由于血液激肽释放酶-激肽系统的激活，以及在中枢神经系统β-肾上腺素能受体长期被阻断的情况下，中枢α-肾上腺素能受体激活后交感神经系统下行抑制作用增强所致。低剂量可乐定所产生的血流动力学变化，可能是由于其中心α-肾上腺素能模拟效应。
