Redox signaling in central neural regulation of cardiovascular function

被引:104
作者
Zimmerman, MC
Davisson, RL
机构
[1] Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Anat & Cell Biol, Iowa City, IA 52245 USA
[2] Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Radiat Oncol, Free Rad & Radiat Biol Program, Iowa City, IA 52245 USA
[3] Univ Iowa, Roy J & Lucille A Carver Coll Med, Cardiovasc Ctr, Iowa City, IA 52245 USA
关键词
renin-angiotensin system; free radicals; CNS; NAD(P)H oxidase; superoxide dismutase;
D O I
10.1016/j.pbiomolbio.2003.11.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
One of the most prominent concepts to emerge in cardiovascular research over the past decade, especially in areas focused on angiotensin II (AngII), is that reactive oxygen species (ROS) are critical signaling molecules in a wide range of cellular processes. Many of the physiological effects of AngII are mediated by ROS, and alterations in AngII-mediated redox mechanisms are implicated in cardiovascular diseases such as hypertension and atherosclerosis. Although most investigations to date have focused on the vasculature as a key player, the nervous system has recently begun to gain attention in this field. Accumulating evidence suggests that ROS have important effects on central neural mechanisms involved in blood pressure regulation, volume homeostasis, and autonomic function, particularly those that involve AngII signaling. Furthermore, oxidant stress in the central nervous system is implicated in the neuro-dysregulation associated with some forms of hypertension and heart failure. The main objective of this review is to discuss the recent progress and prospects for this new field of central redox signaling in cardiovascular regulation, while also addressing the molecular tools that have spurred it forward. (C) 2003 Elsevier Ltd. All rights reserved.
引用
收藏
页码:125 / 149
页数:25
相关论文
共 164 条
[1]
Transduction of murine cerebellar neurons with recombinant FIV and AAV5 vectors [J].
Alisky, JM ;
Hughes, SM ;
Sauter, SL ;
Jolly, D ;
Dubensky, TW ;
Staber, PD ;
Chiorini, JA ;
Davidson, BL .
NEUROREPORT, 2000, 11 (12) :2669-2673
[2]
Localization and function of angiotensin AT1 receptors [J].
Allen, AM ;
Zhuo, JL ;
Mendelsohn, FAO .
AMERICAN JOURNAL OF HYPERTENSION, 2000, 13 (01) :31S-38S
[3]
Nitric oxide regulates NMDA-driven GABAergic inputs to type I neurones of the rat paraventricular nucleus [J].
Bains, JS ;
Ferguson, AV .
JOURNAL OF PHYSIOLOGY-LONDON, 1997, 499 (03) :733-746
[4]
BAINS JS, 1994, REGUL PEPTIDES, V50, P53
[5]
Endothelial dysfunction in chronic myocardial infarction despite increased vascular endothelial nitric oxide synthase and soluble guanylate cyclase expression -: Role of enhanced vascular superoxide production [J].
Bauersachs, J ;
Bouloumié, A ;
Fraccarollo, D ;
Hu, K ;
Busse, R ;
Ertl, G .
CIRCULATION, 1999, 100 (03) :292-298
[6]
BEYER W, 1991, PROG NUCLEIC ACID RE, V40, P221
[7]
BIANCA VD, 1999, J BIOL CHEM, V274, P15493
[8]
Blomer U, 1997, J VIROL, V71, P6641
[9]
THE RENIN-ANGIOTENSIN SYSTEM IN THE BRAIN - AN UPDATE 1993 [J].
BUNNEMANN, B ;
FUXE, K ;
GANTEN, D .
REGULATORY PEPTIDES, 1993, 46 (03) :487-509
[10]
Brain protein oxidation in age-related neurodegenerative disorders that are associated with aggregated proteins [J].
Butterfield, DA ;
Kanski, J .
MECHANISMS OF AGEING AND DEVELOPMENT, 2001, 122 (09) :945-962