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首页> 外文期刊>American Journal of Physiology >Pregnancy attenuates uterine artery pressure-dependent vascular tone: role of PKC/ERK pathway.
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Pregnancy attenuates uterine artery pressure-dependent vascular tone: role of PKC/ERK pathway.

机译：怀孕减弱子宫动脉压力依赖性血管紧张度：PKC / ERK通路的作用。

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The mechanisms of adaptation of uterine artery vascular tone to pregnancy are not fully understood. The present study tested the hypothesis that pregnancy decreases the PKC-mediated Ca(2+) sensitivity of the contractile process and attenuates myogenic tone in resistance-sized uterine arteries. In pressurized uterine arteries from nonpregnant (NPUA) and near-term pregnant (PUA) sheep, we measured, simultaneously in the same tissue, vascular diameter and vessel wall intracellular Ca(2+) concentration ([Ca(2+)](i)) as a function of intraluminal pressure. In both NPUA and PUA, membrane depolarization with KCl caused a rapid increase in [Ca(2+)](i) and a decrease in diameter. A pressure increase from 20 to 100 mmHg resulted in a transient increase in diameter that was associated with an increase in [Ca(2+)](i), followed by myogenic contractions in the absence of further changes in [Ca(2+)](i). In addition, activation of PKC by phorbol 12,13-dibutyrate induced a decrease in diameter in the absence of changesin [Ca(2+)](i). Pressure-dependent myogenic responses were significantly decreased in PUA compared with NPUA. However, pressure-induced increases in [Ca(2+)](i) were not significantly different between PUA and NPUA. The ratio of changes in diameter to changes in [Ca(2+)](i) was significantly greater for pressure-induced contraction of NPUA than that of PUA. Inhibition of PKC by calphostin C significantly attenuated the pressure-induced vascular tone and eliminated the difference of myogenic responses between NPUA and PUA. In contrast, the MAPKK (MEK) inhibitor PD-098059 had no effect on NPUA but significantly enhanced myogenic responses of PUA. In the presence of PD-098059, there was no difference in pressure-induced myogenic responses between NPUA and PUA. The results suggest that pregnancy downregulates pressure-dependent myogenic tone of the uterine artery, which is partly due to increased MEK/ERK activity and decreased PKC signal pathway leading to a decrease in Ca(2+) sensitivity of myogenic mechanism inthe uterine artery during pregnancy.
机译：子宫动脉血管张力适应妊娠的机制尚未完全了解。本研究检验了以下假设：怀孕可降低PKC介导的Ca（2+）收缩过程的敏感性，并减弱抵抗力大小的子宫动脉中的肌原性张力。在来自非妊娠（NPUA）和近期妊娠（PUA）绵羊的加压子宫动脉中，我们同时在同一组织中测量了血管直径和血管壁细胞内Ca（2+）浓度（[Ca（2 +）]（i ））作为腔内压力的函数。在NPUA和PUA中，用KCl进行的膜去极化会导致[Ca（2 +）]（i）的快速增加和直径的减小。压力从20毫米汞柱增加到100毫米汞柱导致直径瞬时增加，这与[Ca（2 +）]（i）的增加有关，随后在[Ca（2+）]没有进一步变化的情况下发生肌源性收缩]（一世）。此外，在无[Ca（2 +）]（i）变化的情况下，佛波醇12,13-二丁酸酯激活PKC导致直径减小。与NPUA相比，PUA的压力依赖性肌源性反应显着降低。但是，压力诱导的[Ca（2 +）]（i）的增加在PUA和NPUA之间没有显着差异。对于压力诱导的NPUA收缩，直径变化与[Ca（2 +）]（i）变化的比率明显大于PUA。钙磷蛋白C对PKC的抑制作用显着减弱了压力诱导的血管紧张度，并消除了NPUA和PUA之间的肌源性反应差异。相反，MAPKK（MEK）抑制剂PD-098059对NPUA无影响，但显着增强了PUA的肌原性反应。在PD-098059的存在下，NPUA和PUA在压力诱导的肌源性反应方面没有差异。结果表明，妊娠下调子宫动脉的压力依赖性肌源性肌张力，这部分是由于增加了MEK / ERK活性和PKC信号通路降低，从而导致孕期子宫动脉中肌形成机制的Ca（2+）敏感性降低。

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