Circulation Research. 2002
Published online before print October 24, 2002, doi: 10.1161/01.RES.0000043501.47934.FA
Published online before print October 24, 2002, doi: 10.1161/01.RES.0000043501.47934.FA
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Submitted on July 30, 2002
Revised on October 10, 2002
Accepted on October 14, 2002
Superoxide Mediates the Actions of Angiotensin II in the Central Nervous System
Matthew C. Zimmerman ;
From the Department of Anatomy and Cell Biology (M.C.Z., E.L., J.A.L., P.S., R.L.D.) and the Free Radical and Radiation Biology Program, Department of Radiation Oncology (M.C.Z., I.M.A., D.R.S., R.L.D.), The University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City.
* To whom correspondence should be addressed. E-mail: robin-davisson{at}uiowa.edu.
Angiotensin II (Ang II) has profound effects in the central nervous system (CNS), including promotion of thirst, regulation of vasopressin secretion, and modulation of sympathetic outflow. Despite its importance in cardiovascular and volume homeostasis, angiotensinergic mechanisms are incompletely understood in the CNS. Recently, a novel signaling mechanism for Ang II involving reactive oxygen species (ROS) has been identified in a variety of peripheral tissues, but the involvement of ROS as second messengers in Ang II-mediated signaling in the CNS has not been reported. The hypothesis that superoxide is a key mediator of the actions of Ang II in the CNS was tested in mice using adenoviral vector-mediated expression of superoxide dismutase (AdSOD). Changes in blood pressure, heart rate, and drinking elicited by injection of Ang II in the CNS were abolished by prior treatment with AdSOD in the brain, whereas the cardiovascular responses to carbachol, another central vasopressor agent, were unaffected. In addition, Ang II stimulated superoxide generation in primary CNS cell cultures, and this was prevented by the Ang II receptor (Ang II type 1 subtype) antagonist losartan or AdSOD. These results identify a novel signaling mechanism mediating the actions of Ang II in the CNS. Dysregulation of this signaling cascade may be important in hypertension and heart failure triggered by Ang II acting in the CNS.
Key words: blood pressure • thirst • reactive oxygen species • renin-angiotensin system • brain
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