CENTRAL ACTIONS OF ANGIOTENSIN IN CARDIOVASCULAR CONTROL - MULTIPLE ROLES FOR A SINGLE PEPTIDE
CENTRAL ACTIONS OF ANGIOTENSIN IN CARDIOVASCULAR CONTROL - MULTIPLE ROLES FOR A SINGLE PEPTIDE
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DOI：
10.1139/y92-103
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发表时间：
1992-05-01
影响因子：
2.1
通讯作者：
WALL, KM
中科院分区：
文献类型：
--
作者：
FERGUSON, AV;WALL, KM
血管紧张素II（ANG II）作为一种激素在外周发挥作用，作用于血管系统、肾上腺和肾脏。此外，ANG II在中枢神经系统中的某些作用是针对心血管控制和体液容量稳态的。血管紧张素II的密集结合位点位于室周器官，这些器官显然具有通过神经回路向心血管中心传递信息的能力。将ANG II微量注射到穹窿下器官（SFO）或最后区（AP）中可产生血压的部位特异性升高。此外，电生理学研究表明，ANG II，在SFO的作用，对神经垂体神经元的活动和催产素和加压素的释放，这可以拮抗ANG II阻滞剂或衰减的SFO病变的深刻影响。从显微注射，电生理和病变的研究表明，复杂的相互作用的中央网站参与心血管控制的机制：SFO，AP，终板的血管器，室旁核和视上核的下丘脑。ANG II不仅是这一中枢情景中的体液信使，而且有证据表明它在特定CNS通路中充当神经递质或神经内分泌物质，表明该肽在中枢心血管控制中具有多种作用。
Angiotensin II (ANG II) acts peripherally as a hormone, with actions on the vasculature, adrenals, and kidney. In addition, certain actions of ANG II in the central nervous system are directed toward cardiovascular control and fluid volume homeostasis. Dense binding sites for ANG II are found at circumventricular organs, which apparently have the ability to relay information to cardiovascular centers via neural circuitry. Microinjection of ANG II into the subfornical organ (SFO) or area postrema (AP) produces site-specific increases in blood pressure. In addition, electrophysiological studies demonstrate profound effects of ANG II, acting at the SFO, on activity of neurohypophysial neurons and release of oxytocin and vasopressin, which can be antagonized by ANG II blockers or attenuated by SFO lesions. Evidence from microinjection, electrophysiological, and lesion studies indicate a complex interaction between central sites involved in mechanisms of cardiovascular control: the SFO, AP, organum vasculosum of the lamina terminalis, and paraventricular and supraoptic nuclei of the hypothalamus. Not only is ANG II a humoral messenger in this central scenario, but evidence suggests it acts as a neurotransmitter or neuroendocrine substance within specific CNS pathways, suggesting multiple roles for this peptide in central cardiovascular control.