Nelson M T, Patlak J B, Worley J F, Standen N B
Department of Pharmacology, University of Vermont, Burlington 05405.
Am J Physiol. 1990 Jul;259(1 Pt 1):C3-18. doi: 10.1152/ajpcell.1990.259.1.C3.
Resistance arteries exist in a maintained contracted state from which they can dilate or constrict depending on need. In many cases, these arteries constrict to membrane depolarization and dilate to membrane hyperpolarization and Ca-channel blockers. We discuss recent information on the regulation of arterial smooth muscle voltage-dependent Ca channels by membrane potential and vasoconstrictors and on the regulation of membrane potential and K channels by vasodilators. We show that voltage-dependent Ca channels in the steady state can be open and very sensitive to membrane potential changes in a range that occurs in resistance arteries with tone. Many synthetic and endogenous vasodilators act, at least in part, through membrane hyperpolarization caused by opening K channels. We discuss evidence that these vasodilators act on a common target, the ATP-sensitive K (KATP) channel that is inhibited by sulfonylurea drugs. We propose the following hypotheses that presently explain these findings: 1) arterial smooth muscle tone is regulated by membrane potential primarily through the voltage dependence of Ca channels; 2) many vasoconstrictors act, in part, by opening voltage-dependent Ca channels through membrane depolarization and activation by second messengers; and 3) many vasodilators work, in part, through membrane hyperpolarization caused by KATP channel activation.
阻力动脉处于持续收缩状态，可根据需要扩张或收缩。在许多情况下，这些动脉会因膜去极化而收缩，因膜超极化和钙通道阻滞剂而扩张。我们讨论了关于膜电位和血管收缩剂对动脉平滑肌电压依赖性钙通道的调节，以及血管舒张剂对膜电位和钾通道的调节的最新信息。我们发现，稳态下的电压依赖性钙通道可以开放，并且在有张力的阻力动脉所出现的膜电位变化范围内对其非常敏感。许多合成和内源性血管舒张剂至少部分地通过开放钾通道引起的膜超极化起作用。我们讨论了这些血管舒张剂作用于一个共同靶点——被磺脲类药物抑制的ATP敏感性钾（KATP）通道的证据。我们提出以下假设来解释目前的这些发现：1）动脉平滑肌张力主要通过钙通道的电压依赖性由膜电位调节；2）许多血管收缩剂部分地通过膜去极化和第二信使激活来开放电压依赖性钙通道起作用；3）许多血管舒张剂部分地通过KATP通道激活引起的膜超极化起作用。
