NO and central cardiovascular control: a simple molecule with a complex story.
NO and central cardiovascular control: a simple molecule with a complex story.
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DOI：
10.1161/01.hyp.0000238142.22799.80
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发表时间：
2006-10
期刊：
影响因子：
8.3
通讯作者：
W. Talman
中科院分区：
文献类型：
--
作者：
W. Talman
1998年诺贝尔生理学或医学奖表彰了罗伯特·福尔奇戈特、路易斯·伊格纳罗和费里德·穆拉德的巨大贡献，因为他们发现了一氧化氮在心血管系统中作为信号分子的作用。Furchgot的早期工作描述了一种血管扩张因子，这种因子是由作用于完整内皮的乙酰胆碱激活的，不仅为随后认识到NO是内皮衍生的松弛因子奠定了基础，而且也是后续许多经典神经递质和NO之间相互作用研究的先兆。一氧化氮合酶(NOS)是合成NO的生物合成酶，目前已鉴定出三种异构体。内皮型一氧化氮合酶(ENOS)和神经型一氧化氮合酶(NNOS)是两种构成酶。在压力感受性传入神经终止的主要部位--孤束核(NTS)中，每一种都已被发现，但每一种或NO本身在通过NTS的压力感受性反射传递中的作用仍存在很大疑问。NTS中iNOS的存在可能表明在发现iNOS的动物中存在应激。为了与NO可能连接递质机制并整合血管和神经功能的可能性保持一致，Waki等人在本期《高血压1》上的工作为通过NO机制在NTS中进行复杂整合以及NO在心血管内稳态紊乱中的作用提供了进一步的证据。这项工作是布里斯托尔大学Paton/Kasparov实验室的最新工作，进一步支持了一系列涉及内皮型一氧化氮合酶产生的NO的转导事件，以及NTS调节血压的其他几种假定的递质。血管紧张素就是这样一种潜在的递质。特别是自从Casto和Phillips的工作以来，人们已经认识到血管紧张素可能在NTs到…的水平上起作用
The 1998 Nobel Prize in Physiology or Medicine recognized the great contributions of Robert Furchgott, Louis Ignarro, and Ferid Murad through “their discoveries concerning nitric oxide as a signaling molecule in the cardiovascular system.” Furchgott’s earlier work describing a vasodilatory factor that was activated by acetylcholine acting on an intact endothelium not only set the stage for subsequent recognition that NO was the endothelium-derived relaxation factor but also acted as a harbinger of much subsequent study of interactions between classic neurotransmitters and NO. Three isoforms of NO synthase (NOS), the biosynthetic enzyme for synthesis of NO, have been identified. Two are constitutive enzymes, endothelial NOS (eNOS) and neuronal NO (nNOS). Each has been identified in the nucleus tractus solitarii (NTS), the primary site of termination of baroreceptor afferent nerves, but the role of each, or for that matter the role of NO itself, in baroreflex transmission through the NTS remains very much in question. The presence of iNOS in the NTS could indicate that there had been stress in animals in which it was found. In keeping with the potential that NO may link transmitter mechanisms and may integrate vascular and neuronal functions, the work by Waki et al in this issue of Hypertension 1 provides further evidence for complex integration through NO mechanisms in the NTS and for contributions of NO in disorders of cardiovascular homeostasis. That work is the latest from the Paton/Kasparov laboratories at the University of Bristol and further supports there being a cascade of transduction events that involve NO derived from eNOS, as well as several additional putative transmitters in NTS regulation of blood pressure. One such potential transmitter is angiotensin. Particularly since the work of Casto and Phillips,2 it has been recognized that angiotensin may act at the level of the NTS to …