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(Circulation Research. 2003;92:1282.)
© 2003 American Heart Association, Inc.

Editorials

Interactions Between Angiotensin II and Baroreflexes in Long-Term Regulation of Renal Sympathetic Nerve Activity

Thomas E. Lohmeier

From the Department of Physiology, University of Mississippi Medical Center, Jackson, Miss.

Correspondence to Thomas E. Lohmeier, PhD, Department of Physiology, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216-4505. E-mail tlohmeier@physiology.umsmed.edu

Key Words: angiotensin • hypertension • baroreflex • sympathetic nervous system • renal nerves

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

There is considerable evidence that the sympathetic nervous system plays an important role in the pathogenesis of hypertension.^1–3 However, the factors that chronically influence sympathetic activity and the precise mechanisms that mediate neurally induced hypertension are unclear. Topics of long-standing interest, but of considerable uncertainty, relate to the potential impact of the renin-angiotensin system and baroreflexes on sympathetic activity in hypertension. Numerous studies have demonstrated that baroreflex function is impaired in hypertension and that angiotensin II (Ang II) acutely stimulates the sympathetic nervous system.^3–6 Despite this wealth of information, it is still unclear whether baroreflex dysfunction and elevated plasma levels of Ang II lead to chronic increases in sympathetic activity that promote hypertension. This uncertainty, in large part, has been due to technical limitations that prevent determination of long-term changes in sympathetic activity, particularly sympathetic activity to the kidneys (as discussed below). In this regard, the study by Barrett et al⁷ in this issue of Circulation Research is especially important for two reasons. First, it establishes a novel experimental technique for directly monitoring renal sympathetic nerve activity, 24 hours per day. Thus, for the first time, an experimental tool has been developed for assessing the critical neural signal from the brain to the kidneys that leads to long-term changes in body fluid volumes and arterial pressure. Second, by clearly establishing the time-dependent changes in renal sympathetic nerve activity during the induction of Ang II hypertension, this study brings to focus the complex interactions between Ang II and the sympathetic nervous . . . [Full Text of this Article]

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