Russo D, Fraser R, Kenyon C J
MRC Blood Pressure Unit, Western Infirmary, Glasgow, UK.
J Hypertens. 1990 Sep;8(9):827-33. doi: 10.1097/00004872-199009000-00006.
Vascular responsiveness was evaluated in perfused mesenteric arteries from rats infused with dexamethasone (2 micrograms/day). Full dose-response curves to noradrenaline, vasopressin and potassium chloride were established. In order to investigate whether prostaglandins or noradrenaline uptake were involved in dexamethasone-induced pressor changes, vascular responses were compared before and during treatment with either indomethacin (a cyclo-oxygenase inhibitor) or desipramine (an inhibitor of neuronal catecholamine uptake). Dexamethasone-treated tissues showed an increased vascular sensitivity to noradrenaline compared with controls; the maximal response was greater and the concentrations of agonist required for a 50% response (EC50) was less in dexamethasone-treated tissues. The responses to vasopressin and potassium chloride were not affected. Systolic blood pressure in dexamethasone-treated rats was not significantly different from that in controls. Indomethacin infusion decreased the vascular responsiveness to noradrenaline in control and dexamethasone-treated rats to a similar degree. Noradrenaline responses after indomethacin treatment were not significantly different in control and dexamethasone-treated tissues. 6-Keto-prostaglandin-F1 alpha output during stimulation with noradrenaline was not affected by dexamethasone. Desipramine lowered pressor responses to noradrenaline at all concentrations and decreased the maximal response in tissues from dexamethasone-treated but not control rats. However, during infusion with desipramine, the EC50 for noradrenaline after dexamethasone was still less than in controls. Dexamethasone at low doses appears to selectively increase vascular sensitivity to noradrenaline in rats at a prehypertensive stage by changing prostaglandin synthesis and, possibly, neuronal uptake of noradrenaline.
对输注地塞米松（2微克/天）的大鼠的灌注肠系膜动脉的血管反应性进行了评估。建立了去甲肾上腺素、血管加压素和氯化钾的完整剂量-反应曲线。为了研究前列腺素或去甲肾上腺素摄取是否参与地塞米松诱导的升压变化，在用吲哚美辛（一种环氧化酶抑制剂）或地昔帕明（一种神经元儿茶酚胺摄取抑制剂）治疗之前和期间比较了血管反应。与对照组相比，地塞米松处理的组织对去甲肾上腺素的血管敏感性增加；在地塞米松处理的组织中，最大反应更大，产生50%反应所需的激动剂浓度（EC50）更低。对血管加压素和氯化钾的反应不受影响。地塞米松处理的大鼠的收缩压与对照组无显著差异。输注吲哚美辛在相似程度上降低了对照组和地塞米松处理大鼠对去甲肾上腺素的血管反应性。吲哚美辛处理后，对照组和地塞米松处理组织中对去甲肾上腺素的反应无显著差异。去甲肾上腺素刺激期间6-酮-前列腺素-F1α的输出不受地塞米松影响。地昔帕明降低了所有浓度下对去甲肾上腺素的升压反应，并降低了地塞米松处理而非对照大鼠组织中的最大反应。然而，在地昔帕明输注期间，地塞米松处理后去甲肾上腺素的EC50仍低于对照组。低剂量地塞米松似乎通过改变前列腺素合成以及可能通过改变去甲肾上腺素的神经元摄取，选择性增加高血压前期大鼠对去甲肾上腺素的血管敏感性。
