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      Exaggerated sympathetic and cardiovascular responses to stimulation of the mesencephalic locomotor region in spontaneously hypertensive rats

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          Abstract

          The data suggest that the exaggerated cardiovascular and sympathetic responses to physical activity characteristic of hypertension are mediated, in part, by augmentations in central command function. These findings identify the central command pathway as a potential target for the treatment of exercise-induced circulatory hyperexcitability in hypertensive individuals.

          Abstract

          The sympathetic and pressor responses to exercise are exaggerated in hypertension. However, the underlying mechanisms causing this abnormality remain to be fully elucidated. Central command, a neural drive originating in higher brain centers, is known to activate cardiovascular and locomotor control circuits concomitantly. As such, it is a viable candidate for the generation of the augmented vascular response to exercise in this disease. We hypothesized that augmentations in central command function contribute to the heightened cardiovascular response to exercise in hypertension. To test this hypothesis, changes in renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) in response to electrical stimulation of mesencephalic locomotor region (MLR; 20–50 μA in 10-μA steps evoking fictive locomotion), a putative component of the central command pathway, were examined in decerebrate, paralyzed normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Tibial nerve discharge during MLR stimulation significantly increased in an intensity-dependent manner in both WKY and SHR but was not different between groups. Stimulation of the MLR evoked significantly larger increases in RSNA and MAP with increasing stimulation intensity in both groups. Importantly, the increases in sympathetic and pressor responses to this fictive locomotion were significantly greater in SHR compared with WKY across all stimulation intensities (e.g., at 50 μA, ΔRSNA: WKY 153±31%, SHR 287±42%; ΔMAP: WKY 87±9 mmHg, SHR 139±7 mmHg). These findings provide the first evidence that central command may be a critical contributor to the exaggerated rise in sympathetic activity and blood pressure during exercise in hypertension.

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          Author and article information

          Journal
          Am J Physiol Heart Circ Physiol
          Am. J. Physiol. Heart Circ. Physiol
          ajpheart
          ajpheart
          AJPHEART
          American Journal of Physiology - Heart and Circulatory Physiology
          American Physiological Society (Bethesda, MD )
          0363-6135
          1522-1539
          6 November 2015
          1 January 2016
          1 January 2017
          : 310
          : 1
          : H123-H131
          Affiliations
          1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas;
          2Department of Health Care Sciences, University of Texas Southwestern Medical Center, Dallas, Texas; and
          3Department of Integrative Physiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan
          Author notes
          Address for reprint requests and other correspondence: M. Mizuno, Dept. of Health Care Sciences, Univ. of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9174 (e-mail: masaki.mizuno@ 123456utsouthwestern.edu ).
          Article
          PMC4796463 PMC4796463 4796463 H-00479-2015
          10.1152/ajpheart.00479.2015
          4796463
          26545711
          Copyright © 2016 the American Physiological Society
          Funding
          Funded by: 100000050 HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)
          Award ID: HL-088422
          Funded by: The Lawson & Rogers Lacy Research Fund in Cardiovascular Disease
          Funded by: Japan Society for the Promotion of Science
          Categories
          Integrative Cardiovascular Physiology and Pathophysiology

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