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(Circulation Research. 2005;97:737.)
© 2005 American Heart Association, Inc.

Editorials

The Regulation of Sympathetic Nerve Activity by Angiotensin II Involves Reactive Oxygen Species and MAPK

Irving H. Zucker, Lie Gao

From the Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha.

Correspondence to Irving H. Zucker, PhD, Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, NE 68198-5850. E-mail izucker@unmc.edu

See related article, pages 772–780

Key Words: autonomic nerve activity • ROS • superoxide • RVLM

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The central regulation of sympathetic nerve activity has been extensively investigated in normal and disease states since the detailed description of the cardiovascular pressor area by Alexander in 1946.¹ This so called "pressor area" we now know to be the rostral ventrolateral medulla (RVLM). The neurons of the RVLM constitute the primary motor neuron pool from which sympathetic projections to the spinal cord arise. Importantly, the RVLM also receives inputs from a variety of integrative areas in the hypothalamus and medulla. The net sympathetic outflow of various cardiovascular reflexogenic areas have a common pathway which exits the brain from the RVLM. In addition to the neural modulation of these reflexes from hard wired areas in the hypothalamus, medulla, and forebrain, it has become increasingly more recognized that autocrine, paracrine, and endocrine influences on these sympathetic neurons are important for the regulation of arterial pressure, myocardial function, salt and water balance, and general cardiovascular homeostasis in the normal resting state and during the extremes of cardiovascular function such as exercise, heart failure, hypertension, etc.^2–5

Neuronal excitability in the RVLM is not only modulated by classical neurotransmitters such as glutamate and gamma amino butyric acid (GABA) but appears also to be regulated by the ubiquitous octapeptide angiotensin II (Ang II).^6–8 In fact, Ang II, in addition to its myriad of cardiovascular and endocrine effects, has been known for many years to modulate sympathetic function at various sites in the central and peripheral nervous systems.⁹ One of the earliest works in this area . . . [Full Text of this Article]

Related Article:

NADPH Oxidase–Derived Superoxide Anion Mediates Angiotensin II–Induced Pressor Effect via Activation of p38 Mitogen–Activated Protein Kinase in the Rostral Ventrolateral Medulla

Samuel H.H. Chan, Kuei-Sen Hsu, Chiung-Chun Huang, Ling-Lin Wang, Chen-Chun Ou, and Julie Y.H. Chan
Circ. Res. 2005 97: 772-780. [Abstract] [Full Text] [PDF]

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