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      Increased Expression of Macrophage Migration Inhibitory Factor in the Nucleus of the Solitary Tract Attenuates Renovascular Hypertension in Rats

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          Abstract

          BACKGROUND

          Macrophage migration inhibitory factor (MIF) is an intracellular inhibitory regulator of the actions of angiotensin II in the central nervous system. Renovascular hypertensive 2-kidney, 1-clip (2K1C) rats have an increased activity of the renin–angiotensin system and a decrease in baroreflex function compared to normotensive (NT) rats. In the present study, we tested the effects of MIF overexpression within the nucleus of the solitary tract (NTS), a key brainstem region for cardiovascular regulation, on the development of hypertension, on baroreflex function, and on water and food intake in 2K1C rats.

          METHODS

          Holtzman NT rats received a silver clip around the left renal artery to induce 2K1C hypertension. Three weeks later, rats were microinjected in the NTS with AAV2-CBA-MIF, to increase the expression of MIF, or with the control vector AAV2-CBA-enhanced green fluorescent protein. Mean arterial pressure (MAP) and heart rate were recorded by telemetry. Baroreflex function was tested, and water and food intake were also measured.

          RESULTS

          Increasing MIF expression in the NTS of 2K1C rats attenuated the development of hypertension, reversed the impairment of baroreflex function, and reduced the increase in water intake. In contrast to 2K1C rats, similar increases in MIF expression in the NTS of NT rats produced no changes in baseline MAP, baroreflex function, or water intake.

          CONCLUSIONS

          These results indicate that an increased expression of MIF within the NTS attenuates the development of hypertension and restores the baroreflex function in 2K1C rats.

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          Author and article information

          Journal
          Am J Hypertens
          Am. J. Hypertens
          ajh
          American Journal of Hypertension
          Oxford University Press (US )
          0895-7061
          1941-7225
          April 2017
          31 January 2017
          01 April 2018
          : 30
          : 4
          : 435-443
          Affiliations
          [1 ] Department of Physiology and Pathology, School of Dentistry, São Paulo State University , Araraquara, São Paulo, Brazil;
          [2 ] Department of Physiology, Ribeirão Preto Medical School, University of São Paulo , Ribeirão Preto, São Paulo, Brazil;
          [3 ] School of Biotechnology, Southern Medical University , Guangzhou, China;
          [4 ] Department of Physiology and Functional Genomics, College of Medicine, University of Florida , Gainesville, Florida, USA.
          Author notes

          Correspondence: Débora Simões de Almeida Colombari ( deborac@ 123456foar.unesp.br ).

          Article
          PMC5861587 PMC5861587 5861587 hpx001
          10.1093/ajh/hpx001
          5861587
          28158469
          44388c76-a155-4a88-bf27-fb8e12e69222
          © American Journal of Hypertension, Ltd 2017. All rights reserved. For Permissions, please email: journals.permissions@oup.com
          History
          : 20 June 2016
          : 02 January 2017
          : 20 October 2016
          Page count
          Pages: 9
          Funding
          Funded by: National Institutes of Health 10.13039/100000002
          Award ID: HL-076803
          Funded by: CNPq
          Award ID: 473108/2011–9
          Award ID: 304918/2011–3
          Funded by: FAPESP
          Award ID: 2011/50770–1
          Award ID: 2015/23467-7
          Categories
          Original Article
          Brain and CNS

          AT1 receptor,2K1C.,hypertension,brainstem,blood pressure,baroreflex,angiotensin II

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