Schlegel P A, Monney M, Brunner H R
Clin Exp Hypertens A. 1985;7(11):1583-96. doi: 10.3109/10641968509073611.
The aim of this study was to assess the pressure response of mesenteric arteries isolated from various hypertensive rat models to the 3 pressor agonists norepinephrine, lysinevasopressin and angiotensin II. The isolated mesenteric arterial beds were perfused with a Krebs-solution and then exposed to increasing doses of the 3 different pressor agents. Compared to Wistar Kyoto controls, spontaneously hypertensive rats exhibited a clearly enhanced vascular response to norepinephrine and lysine vasopressin but not to angiotensin II. In animals with hypertension produced by angiotensin II continuously released by an osmotic micropump, the vascular response to lysine vasopressin and angiotensin II was increased while that to norepinephrine was unchanged. Rats rendered hypertensive by the administration of deoxycorticosterone and salt exhibited an increased vascular response exclusively to angiotensin II. In all models taken together, the magnitude of the vascular response to norepinephrine and lysine vasopressin was related to the blood pressure of the intact animal but this was not the case for angiotensin II. These observations are not incompatible with the concept that changes in the vascular response are predominantly due to structural changes of the vascular wall. However, they suggest that more specific alterations of responsiveness of the vascular smooth muscle must also take place.
本研究的目的是评估从各种高血压大鼠模型分离出的肠系膜动脉对三种升压激动剂去甲肾上腺素、赖氨酸加压素和血管紧张素II的压力反应。将分离出的肠系膜动脉床用 Krebs 溶液灌注,然后暴露于递增剂量的三种不同升压剂中。与 Wistar Kyoto 对照相比,自发性高血压大鼠对去甲肾上腺素和赖氨酸加压素的血管反应明显增强,但对血管紧张素 II 无增强反应。在由渗透微型泵持续释放血管紧张素 II 所致高血压的动物中,对赖氨酸加压素和血管紧张素 II 的血管反应增强,而对去甲肾上腺素的反应不变。给予脱氧皮质酮和盐所致高血压的大鼠仅对血管紧张素 II 的血管反应增强。综合所有模型来看,对去甲肾上腺素和赖氨酸加压素的血管反应幅度与完整动物的血压有关,但血管紧张素 II 并非如此。这些观察结果与血管反应变化主要归因于血管壁结构变化的概念并不矛盾。然而,它们表明血管平滑肌反应性也必定发生了更具体的改变。