Ayada C, Toru Ü, Korkut Y
Department of Physiology, Medical Faculty, Dumlupınar University, Kütahya, Turkey.
Department of Chest Diseases, Medical Faculty, Dumlupınar University, Kütahya, Turkey.
Hippokratia. 2015 Apr-Jun;19(2):99-108.
Exaggerated cardiovascular response to acute and chronic stresses increases the risk for hypertension and cardiovascular disease. Stress also can be broadly defined as a disruption of homeostasis. The re-establishment and maintenance of homeostasis entail the coordinated activation and control of neuroendocrine and autonomic stress systems. Stressor-related information from all major sensory systems is conveyed to the brain. Brain activates neural and neuroendocrine systems to minimize the harmful effects of stress. Stress is generally thought to contribute to the development of hypertension. On the other hand, the evidence is still inconclusive. It is generally accepted that stress-induced hypertension occurs because of increases in sympathoadrenal activity, which enhances vascular tone, but complete α-adrenoreceptor blockade cannot prevent the long-lasting vasoconstriction induced by sympathetic nerve stimulation. That is why it is suggested that sympathetic nerve-mediated vasoconstriction may also be mediated by factors other than catecholamines. In this review, we aim to present the relationship between blood pressure effectors and stress altogether, along with evaluating the relationship between stress and blood pressure. In this respect, we have identified topics to explain the relationship between stress and the renin angiotensin aldosterone system, glucocorticoids, endothelial nitric oxide, endothelin-1 and L-type Ca2+ channels. Hippokratia 2015; 19 (2): 99-108.
对急性和慢性应激的过度心血管反应会增加患高血压和心血管疾病的风险。应激也可被广义地定义为内稳态的破坏。内稳态的重新建立和维持需要神经内分泌和自主应激系统的协同激活与控制。来自所有主要感觉系统的与应激源相关的信息会被传递到大脑。大脑激活神经和神经内分泌系统以将应激的有害影响降至最低。一般认为应激会促成高血压的发展。另一方面，证据仍不确凿。人们普遍认为应激诱导的高血压是由于交感肾上腺活动增加所致，这会增强血管张力，但完全的α-肾上腺素能受体阻断并不能预防交感神经刺激所诱导的持久血管收缩。这就是为什么有人提出交感神经介导的血管收缩也可能由儿茶酚胺以外的因素介导。在本综述中，我们旨在全面阐述血压效应器与应激之间的关系，同时评估应激与血压之间的关系。在这方面，我们确定了一些主题来解释应激与肾素-血管紧张素-醛固酮系统、糖皮质激素、内皮一氧化氮、内皮素-1和L型钙通道之间的关系。《希波克拉底》2015年；19(2):99 - 108。
