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      Enhanced angiotensin-converting enzyme activity and systemic reactivity to angiotensin II in normotensive rats exposed to a high-sodium diet

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          A high salt diet is associated with reduced activity of the renin–angiotensin–aldosterone system (RAAS). However, normotensive rats exposed to high sodium do not show changes in systemic arterial pressure. We hypothesized that, despite the reduced circulating amounts of angiotensin II induced by a high salt diet, the cardiovascular system’s reactivity to angiotensin II is increased in vivo, contributing to maintain arterial pressure at normal levels. Male Wistar rats received chow containing 0.27% (control), 2%, 4%, or 8% NaCl for six weeks. The high-sodium diet did not lead to changes in arterial pressure, although plasma levels of angiotensin II and aldosterone were reduced in the 4% and 8% NaCl groups. The 4% and 8% NaCl groups showed enhanced pressor responses to angiotensin I and II, accompanied by unchanged and increased angiotensin-converting enzyme activity, respectively. The 4% NaCl group showed increased expression of angiotensin II type 1 receptors and reduced expression of angiotensin II type 2 receptors in the aorta. In addition, the hypotensive effect of losartan was reduced in both 4% and 8% NaCl groups. In conclusion these results explain, at least in part, why the systemic arterial pressure is maintained at normal levels in non-salt sensitive and healthy rats exposed to a high salt diet, when the functionality of RAAS appears to be blunted, as well as suggest that angiotensin II has a crucial role in the vascular dysfunction associated with high salt intake, even in the absence of hypertension.

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          Author and article information

          Vascul Pharmacol
          Vascul. Pharmacol.
          Vascular pharmacology
          18 February 2016
          07 December 2013
          February 2014
          17 August 2017
          : 60
          : 2
          : 67-74
          [a ]Department of Pharmacology, Universidade Federal do Paraná, Curitiba, PR, Brazil
          [b ]Institute of Biological Sciences, Medical and Health, Universidade Paranaense, Umuarama, PR, Brazil
          [c ]Department of Medicine, Georgia Health Sciences University, Augusta, GA, USA
          [d ]Department of Physiology, Georgia Health Sciences University, Augusta, GA, USA
          [e ]Laboratory of Cardiovascular Pharmacology, Department of Pharmacology, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil
          Author notes
          [* ]Corresponding author at: Universidade Federal de Santa Catarina, Department of Pharmacology, Laboratory of Cardiovascular Pharmacology, Campus Universitário, Trindade, Block D/CCB, Florianópolis, SC, 88049-900, Brazil. Tel.: +55 48 3721 4847; fax: +55 48 3721 9813., j.e.silva.santos@ 123456ufsc.br (J.E. da Silva-Santos)
          PMC5560024 PMC5560024 5560024 nihpa757707


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