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首页> 外文期刊>American Journal of Physiology >The stress of maternal separation causes misprogramming in the postnatal maturation of rat resistance arteries
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The stress of maternal separation causes misprogramming in the postnatal maturation of rat resistance arteries

机译：母体分离的应力导致大鼠抗性动脉出生后成熟的误报

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摘要

We examined the effect of stress in the first 2 wk of life induced by brief periods of daily maternal separation on developmental programming of rat small resistance mesenteric arteries (MAs). In MAs of littermate controls, mRNAs encoding mediators of vasoconstriction, including the aia-adrenergic receptor, smooth muscle myosin heavy chain, and CPI-17, the inhibitory subunit of myosin phosphatase, increased from after birth through sexual [postnatal day (PND) 35] and full maturity, up to ~80-fold, as measured by quantitative PCR. This was commensurate with two- to fivefold increases in maximum force production to KC1 depolarization, calcium, and the a-adrenergic agonist phenylephrine, and increasing systolic blood pressure. Rats exposed to maternal separation stress as neonates had markedly accelerated trajectories of maturation of arterial contractile gene expression and function measured at PND 14 or PND21 (weaning), 1 wk after the end of the stress protocol. This was suppressed by the a-adrenergic receptor blocker terazosin (0.5 mg-kg ip^-day"1), indicating dependence on stress activation of sympathetic signaling. Due to the continued maturation of MAs in control rats, by sexual maturity (PND35) and into adulthood, no differences were observed in arterial function or response to a second stressor in rats stressed as neonates. Thus early life stress misprograms resistance artery smooth muscle, increasing vasoconstrictor function and blood pressure. This effect wanes in later stages, suggesting plasticity during arterial maturation. Further studies are indicated to determine whether stress in different periods of arterial maturation may cause misprogramming persisting through maturity and the potential salutary effect of a-adrenergic blockade in suppression of this response.
机译：我们在日常孕产病患者小抗性肠系膜（MAS）的发育规划中，在日常孕产妇分离的前期诱导的前2周诱导的生命中致力于压力的影响。在凋落物对照的MAS中，编码血管收缩介质的MRNA，包括AIA - 肾上腺素能受体，平滑肌肌蛋白重链和CPI-17，肌蛋白酶磷酸酶的抑制亚基，从出生后通过性（产后日（PND）35 [通过定量PCR测量，全成熟，高达〜80倍。这与最大力产量的最大力量产生的2至五倍相称，对KC1去极化，钙和A-肾上腺素能激动剂去氧肾上腺素，并增加收缩压。暴露于孕产妇分离应力的大鼠作为新生儿在应力方案结束后在PND 14或PND21（断奶）中测量的动脉收缩基因表达和测量的函数明显加速了术的轨迹。 A-肾上腺素能受体阻滞剂抑制唑嗪（0.5mg-kg IP -day“1）抑制，表明对交感神经信号传导的应激活化的依赖性。由于对照大鼠中的MAS持续成熟，通过性成熟（PND35）进入成年期，在动脉函数中没有观察到差异或对作为新生儿的大鼠的第二个压力响应。因此，早期寿命压力误导性耐受动脉平滑肌，增加血管收缩功能和血压。这种效果在以后的阶段，暗示可塑性动脉成熟。表明进一步的研究以确定各种动脉成熟时期的应激是否可能导致误导性通过成熟度和α-肾上腺素能阻滞抑制这种反应的潜在的良好作用。

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