Thompson L P, Bruner C A, Lamb F S, King C M, Webb R C
Am J Cardiol. 1987 Jan 23;59(2):29A-34A. doi: 10.1016/0002-9149(87)90173-1.
Numerous studies have focused on functional vascular changes that characterize the hypertensive state. Recent evidence that suggests that increased vascular reactivity in hypertension is due to changes in the delivery of activator Ca++ through channels in the cell membrane will be reviewed. The primary evidence supporting this hypothesis comes from studies that characterize the effects of Ca++-free solution and calcium channel blockers on contractile properties of isolated vascular smooth muscle. In the present study, experiments were performed to investigate the role of Ca++ influx in vascular contractions produced by interventions that cause membrane depolarization. Isometric tension development in helical strips of carotid arteries from stroke-prone spontaneously hypertensive rats in response to elevated K+ and tetraethylammonium chloride was greater than that in carotid arteries from Wistar-Kyoto normotensive rats. The rate of tension development to K+-free solution in carotid arteries from stroke-prone spontaneously hypertensive rats was faster than in Wistar-Kyoto normotensive rat arteries. Contractile responses to all 3 depolarizing interventions were reduced in arterial strips incubated in Ca++-free solution containing the chelator ethylene glycol bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid and in arterial strips treated with the Ca++ channel blocker verapamil. These results are consistent with the hypothesis that constrictor stimuli that produce membrane depolarization cause an opening of Ca++ channels in the plasma membrane that are sensitive to the organic channel blockers. Further, a change in Ca++ permeability or membrane depolarizing mechanisms contributes to increased contractile responsiveness in carotid arteries of stroke-prone spontaneously hypertensive rats.
众多研究聚焦于高血压状态下具有特征性的功能性血管变化。本文将综述近期的证据，这些证据表明高血压时血管反应性增加是由于激活剂钙离子通过细胞膜通道的转运发生了改变。支持这一假说的主要证据来自于对无钙溶液和钙通道阻滞剂对离体血管平滑肌收缩特性影响的研究。在本研究中，进行了实验以探究钙离子内流在由导致膜去极化的干预措施所引发的血管收缩中的作用。易患中风的自发性高血压大鼠颈总动脉螺旋条对高钾和四乙铵氯化物的等长张力发展大于Wistar-Kyoto正常血压大鼠的颈总动脉。易患中风的自发性高血压大鼠颈总动脉对无钾溶液的张力发展速率比Wistar-Kyoto正常血压大鼠的动脉更快。在含有螯合剂乙二醇双（β-氨基乙基醚）N,N,N',N'-四乙酸的无钙溶液中孵育的动脉条以及用钙通道阻滞剂维拉帕米处理的动脉条中，对所有三种去极化干预的收缩反应均降低。这些结果与以下假说一致，即产生膜去极化的收缩刺激会导致质膜上对有机通道阻滞剂敏感的钙离子通道开放。此外，钙离子通透性或膜去极化机制的改变有助于易患中风的自发性高血压大鼠颈总动脉收缩反应性的增加。
