The reaction to thromboxane thromboxane A_2 in smooth muscle cells

为了研究血管内皮细胞对血栓素A_2的反应，我们研究了血小板对血栓素A_2的反应。用尼索地平研究细胞外液Ca~(2+)~(2+)进入血小板的调节。在CaCl2存在下，尼索地平或赋形剂加入呋喃西林负载的血小板，同时加入激活剂、血栓素A_2激动剂(U46619)或凝血酶。尼索地平可抑制U46619引起的[Ca~(2+)]i升高，但不能抑制凝血酶引起的[Ca~(2+)]_i升高。当无钙介质中加入CaCl2后，尼索地平可抑制由U46619引起的[Ca~(2+)]i升高，但不能抑制凝血酶引起的升高。尼索地平显著抑制U46619诱导的血小板聚集和分泌，但对凝血酶的反应无影响。这些数据表明，血小板膜上的Ca~(2+)内流受两种或两种以上钙通道的调节，包括血栓素A_2激活通道和凝血酶激活通道。尼索地平仅阻断前一种通道。

To study the reaction thromboxane A_2 in smooth muscle cells, we studied the reaction to thromboxane A_2 in platelets. The regulation of extracelluler Ca^<2+> entry into platelets was studied using nisoldipine. Nisoldipine or vehicle was added to fura2-loaded-platelets in the presence of CaCl_2 and an activator, a thromboxane A_2 agonist (U46619) or thrombin, was also added. In the other experiments, CaCl_2 was added after the activator to platelet samples containing EDTA.The U46619-evoked increase of [Ca^<2+>] i was suppressed by nisoldipine, but the thrombin-evoked [Ca^<2+>] i increase was not suppressed. When CaCl_2 was added to Ca^<2+>-free medium after platelet the activation, the increase of [Ca^<2+>] i due to U46619 was suppressed by nisoldipine, but not that due to thrombin. In addition, nisoldipine significantly suppressed platelet aggregation and secretion induced by U46619, but had no effect on the response to thrombin. These data suggest that Ca^<2+> entry through the platelet membrane is regulated by two or more types of Ca^<2+> channeles, including thromboxane A_2-activated and thrombin-activated channels. Only the former type of channel was blocked by nisoldipine.