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1 Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE, USA
* To whom correspondence should be addressed. E-mail: izucker{at}unmc.edu.
Chronic heart failure (CHF) is often associated with sympatho-excitation and blunted arterial baroreflex function. These phenomena have been causally linked to elevated central angiotensin II (Ang II) mechanisms. Recent studies have shown that NAD(P)H oxidase-derived reactive oxidant species (ROS) are important mediators of Ang II signaling, and therefore might play an essential role in the above interactions. The aims of this study were to determine whether central subchronic infusion of Ang II in normal animals have effects on O2- production and expression of NAD(P)H oxidase subunits as well as AT1 receptors in the rostral ventrolateral medulla (RVLM). 24 male New Zealand White rabbits were divided into four groups and separately received a subchronic intracerebroventricular (icv) infusion of saline alone, Ang II alone, Ang II + losartan, and losartan alone for 1 week. On the seventh day of icv infusion, the mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded, and the arterial baroreflex sensitivity was evaluated in the conscious state. We found that (1) Ang II significantly increased baseline RSNA (161.9%, P < 0.05), the mRNA and protein expression of AT1 receptor (mRNA: 66.7%, P < 0.05; protein 85.1%, P < 0.05) and NAD(P)H oxidase subunits (mRNA: 120.0% - 200.0%-fold, P < 0.05; protein: 90.9%- 197.0%, P < 0.05) and O2- production (83.2%, P < 0.05) in the RVLM. In addition the impaired baroreflex control of HR (Gainmax reduced by 48.2%, P < 0.05) and RSNA (Gainmax reduced by 53.6%, P < 0.05) by Ang II were completely abolished by losartan; (2) Losartan significantly decreased the baseline RSNA (-49.5%, P < 0.05) and increased the baroreflex control of HR (Gainmax increased by 64.8%, P < 0.05) and RSNA (Gainmax increased by 67.9%, P < 0.05), but had no significant effects on mRNA and protein expression of AT1 receptor and NAD(P)H oxidase subunits and O2- production in the RVLM. These data suggest that, in normal rabbits, NAD(P)H oxidase-derived ROS play an important role in the modulation of sympathetic activity and arterial baroreflex function by subchronic central treatment of exogenous Ang II via the AT1 receptor.
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