TY - JOUR
T1 - Redox signaling in central neural regulation of cardiovascular function
AU - Zimmerman, Matthew C.
AU - Davisson, Robin L.
N1 - Funding Information:
Original research findings of the authors that are incorporated into this review were supported by grants from the National Institutes of Health (HL-63887 and HL-14388 to R.L.D.) and the American Heart Association (0030017N to R.L.D.; 0310039Z to M.C.Z). The authors would like to thank Timothy Lindley for valuable discussions and input, and Paul Reimann for his expert assistance with the illustration.
PY - 2004
Y1 - 2004
N2 - 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.
AB - 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.
KW - CNS
KW - Free radicals
KW - NAD(P)H oxidase
KW - Renin-angiotensin system
KW - Superoxide dismutase
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U2 - 10.1016/j.pbiomolbio.2003.11.009
DO - 10.1016/j.pbiomolbio.2003.11.009
M3 - Review article
C2 - 14769433
AN - SCOPUS:1242321407
SN - 0079-6107
VL - 84
SP - 125
EP - 149
JO - Progress in Biophysics and Molecular Biology
JF - Progress in Biophysics and Molecular Biology
IS - 2-3
ER -