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Hypoxia-regulated catecholamine secretion in chromaffin cells

机译:磷脂细胞中缺氧调节的儿茶酚胺分泌

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Adrenal catecholamine (CAT) secretion is a general physiological response of animals to environmental stressors such as hypoxia. This represents an important adaptive mechanism to maintain homeostasis and protect vital organs such as the brain. In adult mammals, CAT secretory responses are triggered by activation of the sympathetic nervous system that supplies cholinergic innervation of adrenomedullary chromaffin cells (AMC) via the splanchnic nerve. In the neonate, the splanchnic innervation of AMC is immature or absent, yet hypoxia stimulates a non-neurogenic CAT secretion that is critical for adaptation to extra-uterine life. This non-neurogenic, hypoxia-sensing mechanism in AMC is gradually lost or suppressed postnatally along a time course that parallels the development of splanchnic innervation. Moreover, denervation of adult AMC results in a gradual return of the direct hypoxia-sensing mechanism. The signaling pathways by which neonatal AMC sense acute hypoxia leading to non-neurogenic CAT secretion and the mechanisms that underlie the re-acquisition of hypoxia-sensing properties by denervated adult AMC, are beginning to be understood. This review will focus on current views concerning the mechanisms responsible for direct acute hypoxia sensing and CAT secretion in perinatal AMC and how they are regulated by innervation during postnatal development. It will also briefly discuss plasticity mechanisms likely to contribute to CAT secretion during exposures to chronic and intermittent hypoxia.
机译:肾上腺儿茶酚胺(猫)分泌是动物对环境压力源的一般生理反应,如缺氧。这代表了维持稳态和保护诸如大脑等重要器官的重要自适应机制。在成年哺乳动物中,猫分泌反应是通过激活同情神经系统的激活,该系统通过肝癌神经供应肾上腺素斑铬细胞(AMC)的胆碱能物质。在新生儿中,AMC的Splanc分泌物是不成熟的或不存在的,但缺氧刺激了非神经源性猫的分泌,这对于适应外尿寿命至关重要。这种非神经发生的,在AMC中的非神经发生的缺氧感测机制在后期逐渐丢失或压制,这是相似的,使SPLICHINCING的发展相似。此外,去除成人的AMC导致直接缺氧感测机制的逐步回报。新生儿AMC感应急性缺氧导致非神经源性猫分泌的信号通路以及基于证明的成人AMC重新获取缺氧感应性质的机制,开始理解。本综述将侧重于目前关于负责围产期AMC直接急性缺氧感应和猫分泌的机制的目的,以及它们在出生后发育期间的支配线调节。它还简要介绍在暴露于慢性和间歇性缺氧期间患有猫分泌的可塑性机制。

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