Shibata S
Blood Vessels. 1987;24(3):104-7. doi: 10.1159/000158679.
Okadaic acid (OA) isolated from black sponge (Halichondria) caused tonic contractions of human umbilical arteries and rabbit aorta both in the presence and absence of Ca2+. This tonic contraction was not affected by Ca2+ chelator, Ca2+ entry blockers and La3+. In addition, the antagonists of alpha-adrenoceptors, histamine, serotonin and ACh receptors had no effect on the OA-induced contraction. High K, ouabain and indomethacin failed to inhibit the response to OA. However, the combination of anaerobic conditions and absence of glucose abolished the response to OA. OA had no effect on the myosin B ATPase and saponin-treated skinned fibers of rabbit aorta. The contractile action of OA may not also be related to calmodulin-related PDE and mitochondrial respiration. In conclusion, although the precise mode of action is not evident at the present time, OA, in its unique pharmacological action--that of producing sustained contraction independent of extracellular Ca2+--may alter the handling of Ca2+ to intracellular store sites.
从黑色海绵(Halichondria)中分离出的冈田酸(OA)在有Ca2+和无Ca2+的情况下均能引起人脐动脉和兔主动脉的强直性收缩。这种强直性收缩不受Ca2+螯合剂、Ca2+通道阻滞剂和La3+的影响。此外,α-肾上腺素能受体拮抗剂、组胺、5-羟色胺和乙酰胆碱受体拮抗剂对OA诱导的收缩均无影响。高钾、哇巴因和吲哚美辛均不能抑制对OA的反应。然而,无氧条件和无葡萄糖的联合作用可消除对OA的反应。OA对兔主动脉的肌球蛋白B ATP酶和皂素处理的去表皮纤维无影响。OA的收缩作用也可能与钙调蛋白相关的磷酸二酯酶和线粒体呼吸无关。总之,虽然目前确切的作用方式尚不清楚,但OA具有独特的药理作用——产生与细胞外Ca2+无关的持续性收缩——可能会改变Ca2+向细胞内储存部位的转运。