Intracellular Ca2+ elevation and contraction due to prostaglandin F2alpha in rat aorta.
Intracellular Ca2+ elevation and contraction due to prostaglandin F2alpha in rat aorta.
复制标题
大鼠主动脉中前列腺素 F2α 导致细胞内 Ca2+ 升高和收缩。
DOI：
10.1016/s0014-2999(97)01415-5
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发表时间：
1997
影响因子：
5
通讯作者：
Rapoport,RM
中科院分区：
文献类型：
--
作者：
Tosun,M;Paul,RJ;Rapoport,RM
检测了前列腺素F2α，以确定（a）其对血管平滑肌细胞内Ca 2+水平（[Ca 2 +]i）和力的影响是否通过激活血栓素A2和/或前列腺素受体介导，以及（B）前列腺素受体介导的收缩中通过L型和非L型Ca 2+通道的Ca 2+内流的相对作用。[Ca2+]在负载Fura-2的大鼠主动脉条中同时测量I和力。血栓素A2受体拮抗剂SQ 29548（[1S]-1a，2b（5Z），3b，4a-7-（3-{2-[（苯基氨基）羰基]肼基甲基）-7-氧代双环-[2.2.1]庚-2-基-5-庚烯酸），阻止前列腺素F2α诱导的平台[Ca 2 +] i升高和力80- 90%，同时消除血栓烷A2受体激动剂引起的这些反应，U46619（9，11-双脱氧-9 α，11 α-甲氧环氧前列腺素F2α）。维拉帕米不抑制前列腺素F2α（+SQ 29548）诱导的平台[Ca 2 +] i升高和力。非选择性阳离子通道阻断剂Ni ~（2+）在维拉帕米存在下，可消除前列腺素F ~（2 α）（+SQ 29548）引起的[Ca ~（2+）]i升高，而收缩仅部分受到抑制。这些结果表明，在大鼠主动脉中，（1）高浓度前列腺素F2α引起的[Ca ~（2+）] i和力的升高主要是血栓素A_2受体激活的结果，（2）前列腺素F2α引起的收缩的前列腺素成分依赖于通过非L型通道的Ca ~（2+）内流。
Prostaglandin F2αwas tested to determine (a) whether its effect on intracellular Ca2+levels ([Ca2+]i) and force in vascular smooth muscle was mediated through activation of the thromboxane A2and/or prostaglandin receptor, and (b) the relative roles of Ca2+influx via L-type and non-L-type Ca2+channels in prostaglandin receptor-mediated contraction. [Ca2+]iand force were measured simultaneously in fura-2-loaded rat aortic strips. The thromboxane A2receptor antagonist, SQ29548 ([1S]-1a,2b(5Z),3b,4a-7-(3-{2-[(phenylamino)carbonyl] hydrazinomethyl)-7-oxobicyclo-[2.2.1]hept-2-yl-5-heptenoic acid), prevented the prostaglandin F2α-induced plateau [Ca2+]ielevation and force by 80–90%, while abolishing these responses due to the thromboxane A2receptor agonist, U46619 (9,11-dideoxy-9α,11α-methanoepoxy prostaglandin F2α). Prostaglandin F2α(+SQ29548)-induced plateau [Ca2+]ielevation and force were not inhibited by verapamil. Ni2+, a non-selective cation channel blocker, in the presence of verapamil, abolished the prostaglandin F2α(+SQ29548)-elevated [Ca2+]i, while the contraction was only partially inhibited. These results suggest that, in rat aorta, (1) elevated [Ca2+]iand force due to high prostaglandin F2αconcentrations largely results from thromboxane A2receptor activation, and (2) the prostaglandin component of the prostaglandin F2α-induced contraction is dependent on Ca2+influx via non-L-type channels.