Driessens M, Vanhoutte P M
Am J Physiol. 1981 Jul;241(1):H91-4. doi: 10.1152/ajpheart.1981.241.1.H91.
Experiments were designed to determine whether or not calcitonin, parathormone, and glucocorticoids have direct effects on the vascular smooth muscle cells of bone blood vessels. Tibias of mongrel dogs were isolated. The arteria nutriens was cannulated and perfused at constant flow with aerated Krebs-Ringer solution (37 degrees C). The perfusion pressure was continuously recorded. In unstimulated preparations calcitonin caused dose-dependent increases in perfusion pressure, indicating that it causes constriction of bone blood vessels. Parathormone did not affect basal perfusion; it did not significantly alter vasoconstrictions caused by the injection of norepinephrine indicating that the hormone has no direct effect on the vascular smooth muscle of bone blood vessels. Hydrocortisone, at low concentrations, augmented the constrictions caused by exogenous norepinephrine and periarterial nerve stimulation; at higher concentrations, hydrocortisone caused a dose-dependent inhibition of the response to adrenergic activation. The depressant effect of hydrocortisone was antagonized by propranolol, suggesting that the glucocorticoid facilitates beta-adrenergic relaxation of the vascular smooth muscle cells by catecholamines.
设计实验以确定降钙素、甲状旁腺激素和糖皮质激素是否对骨血管的血管平滑肌细胞有直接作用。分离杂种狗的胫骨。将滋养动脉插管，并用充氧的 Krebs-Ringer 溶液（37℃）以恒定流量灌注。连续记录灌注压力。在未受刺激的标本中，降钙素导致灌注压力呈剂量依赖性增加，表明它会引起骨血管收缩。甲状旁腺激素不影响基础灌注；它不会显著改变由注射去甲肾上腺素引起的血管收缩，这表明该激素对骨血管的血管平滑肌没有直接作用。低浓度的氢化可的松增强了外源性去甲肾上腺素和动脉周围神经刺激引起的收缩；在较高浓度下，氢化可的松导致对肾上腺素能激活的反应呈剂量依赖性抑制。普萘洛尔拮抗了氢化可的松的抑制作用，表明糖皮质激素通过儿茶酚胺促进血管平滑肌细胞的β-肾上腺素能舒张。
