Department of Pharmacology, The University of Vermont Medical Research Facility, 55A South Park Drive, Colchester, VT 05446, USA.
Trends Cardiovasc Med. 1993 Mar-Apr;3(2):54-60. doi: 10.1016/1050-1738(93)90037-7.
Membrane hyperpolarization through activation of potassium channels in arterial smooth muscle appears to be an effective mechanism to dilate arteries. Conversely, membrane depolarization through inhibition of potassium channels can lead to vasoconstriction. Here, I briefly review the roles of Ca(2+)-activated K(+) (K(Ca)) channels and ATP-sensitive K(+) (K(ATP)) channels in the control of arterial smooth muscle function. K(Ca) channels regulate arterial tone in response to changes in intravascular pressure and possibly to a variety of vasoconstrictors. K(ATP) channels respond to changes in the cellular metabolic state and are targets of a variety of synthetic and endogenous vasodilators.
通过激活动脉平滑肌中的钾通道使膜超极化，这似乎是一种扩张血管的有效机制。相反，通过抑制钾通道使膜去极化会导致血管收缩。在这里，我简要回顾一下钙激活钾（K(Ca)）通道和 ATP 敏感性钾（K(ATP)）通道在控制动脉平滑肌功能中的作用。K(Ca)通道调节血管张力以响应血管内压力的变化，并且可能响应各种血管收缩剂。K(ATP)通道响应细胞代谢状态的变化，并且是各种合成和内源性血管扩张剂的作用靶点。
