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首页> 外文期刊>American Journal of Physiology >Amphetamine-induced sensitization of hypertension and lamina terminalis neuroinflammation
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Amphetamine-induced sensitization of hypertension and lamina terminalis neuroinflammation

机译：Amphetamine诱导的高血压和Lamina Agranceis神经炎炎症的致敏

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Neuroplasticity is an intrinsic capacity of the nervous system that allows animals to make behavioral and physiological adaptations to environmental challenges. However, in some cases, behavioral and physiological plasticity can promote disease states. Recent work from our laboratory (17, 18) has implicated a role for neuroplasticity in the etiology of essential hypertension. That is, events that generally are regarded as challenges (i.e., stressors) will produce hypertensive response sensitization (HTRS), where prior exposure to a stressor can make animals susceptible to developing greater hypertension to subsequent hypertensinogenic challenges. For example, administration of subpressor doses of angiotensin II (ANG II) or aldosterone, consumption of a high-fat diet, or social defeat exacerbate blood pressure (BP) responses to a slow-pressor dose of ANG II delivered following a delay after the stressor exposure has concluded (31-34). HTRS has been linked to neuroplasticity in the neural network that regulates sympathetic tone and BP control (17, 18).
机译：神经塑性是神经系统的内在能力，使动物能够对环境挑战做出行为和生理适应性。然而，在某些情况下，行为和生理可塑性可以促进疾病状态。我们实验室的最新工作（17,18）对神经塑性在必需高血压的病因中致力于神经塑性的作用。也就是说，通常被视为挑战（即，压力源）的事件将产生高血压反应敏化（HTR），其中前提暴露于压力源，可以使动物易于发展更大的高血压症以随后的高血管生成挑战。例如，血管紧张素II（Ang II）或醛固酮，高脂饮食的消费或社会失败加剧血压（BP）对慢性压力剂量的血压（BP）的施用给予血管紧张素的剂量，或者血压加剧了压力源暴露已经结束（31-34）。 HTRS与神经网络中的神经塑性相关联，该神经网络中调节交感神经音调和BP控制（17,18）。

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