Quast U
Department of Pharmacology, University of Tübingen, Germany.
Trends Pharmacol Sci. 1993 Sep;14(9):332-7. doi: 10.1016/0165-6147(93)90006-6.
During the past decade, a group of chemically heterogeneous compounds known as the K+ channel openers has emerged. These compounds open a certain class of K+ channels (ATP-sensitive K+ channels) in the sarcolemma of vascular smooth muscle cells, which leads to hyperpolarization of the cell membrane and relaxation of the tissue. The mechanisms by which hyperpolarization affects smooth muscle contraction and contractility can thus be examined. Hyperpolarization induced by these K+ channel openers prevents Ca2+ entry through voltage-operated Ca2+ channels. Surprisingly, and by mechanisms not yet defined, hyperpolarization of the cell also reduces agonist-induced accumulation of inositol 1,4,5-trisphosphate (and consequently, Ca2+ mobilization from intracellular stores), and the Ca2+ sensitivity of the contractile apparatus. In addition, recent evidence reviewed here by Ulrich Quast suggests that the K+ channel openers possess further mechanisms of vasorelaxation not linked to the opening of plasmalemmal K+ channels.
在过去十年中，出现了一类化学性质各异的化合物，称为钾通道开放剂。这些化合物能打开血管平滑肌细胞质膜中某一类钾通道（ATP敏感性钾通道），导致细胞膜超极化，组织松弛。由此可以研究超极化影响平滑肌收缩和收缩性的机制。这些钾通道开放剂诱导的超极化可阻止钙离子通过电压门控钙通道进入。令人惊讶的是，通过尚未明确的机制，细胞的超极化还会减少激动剂诱导的肌醇1,4,5 -三磷酸的积累（进而减少细胞内钙库的钙动员）以及收缩装置对钙离子的敏感性。此外，乌尔里希·夸斯特在此回顾的最新证据表明，钾通道开放剂具有与质膜钾通道开放无关的其他血管舒张机制。
