Busse R
Z Kardiol. 1984;73 Suppl 2:63-9.
In this short review some aspects of our current knowledge of the cellular processes which are involved in the regulation of vascular tone are discussed. We describe at first the structural components of the contractile apparatus in the vascular smooth muscle and discuss then the calcium-dependent mechanisms that regulate contractile protein activity. Phosphorylation of the 20.000-Dalton-myosin light chain is described as one of the key events in the regulation of the smooth muscle activity. However, mechanisms complementary to the primary effect of myosin phosphorylation are also considered. The differences in calcium modulation of contractile processes between striated and smooth muscle are emphasized. The activation of vascular smooth muscle through graded depolarization and/or action potential and the excitation-contraction coupling as a result of an increase of myoplasmic free calcium concentration is described. The concept of calcium channels which open by agonists acting at the membrane receptors (receptor-operated channels) without any change in membrane potential is presented. Finally, we discuss the different ways by which the level of intracellular calcium as the main factor controlling the contractility of vascular smooth muscle can be reduced. However, other mechanisms, e.g. changes in the sensitivity of the contractile proteins at a given calcium concentration must also be considered as a mechanism of relaxation.
在这篇简短的综述中，我们讨论了当前关于参与血管张力调节的细胞过程的一些知识。我们首先描述血管平滑肌收缩装置的结构组成部分，然后讨论调节收缩蛋白活性的钙依赖性机制。20,000道尔顿肌球蛋白轻链的磷酸化被描述为平滑肌活动调节中的关键事件之一。然而，也考虑了与肌球蛋白磷酸化主要作用互补的机制。强调了横纹肌和平滑肌收缩过程中钙调节的差异。描述了通过分级去极化和/或动作电位激活血管平滑肌以及由于肌浆游离钙浓度增加而导致的兴奋-收缩偶联。提出了由作用于膜受体的激动剂打开的钙通道（受体操纵通道）的概念，而膜电位没有任何变化。最后，我们讨论了降低作为控制血管平滑肌收缩性主要因素的细胞内钙水平的不同方式。然而，其他机制，例如在给定钙浓度下收缩蛋白敏感性的变化，也必须被视为一种舒张机制。
