title: Enhanced angiotensin-converting enzyme activity and systemic reactivity to angiotensin II in normotensive rats exposed to a high-sodium diet.
abstract: 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.
authors: Department of Pharmacology, Universidade Federal do Paraná, Curitiba, PR, Brazil; Department of Physiology, Georgia Health Sciences University, Augusta, GA, USA.
authors: Sandra
authors: S
authors: Crestani
authors: Institute of Biological Sciences, Medical and Health, Universidade Paranaense, Umuarama, PR, Brazil.
authors: Arquimedes
authors: A
authors: Gasparotto Júnior
authors: Department of Pharmacology, Universidade Federal do Paraná, Curitiba, PR, Brazil.
authors: Maria C A
authors: MC
authors: Marques
authors: Department of Medicine, Georgia Health Sciences University, Augusta, GA, USA.
authors: Jennifer C
authors: JC
authors: Sullivan
authors: Department of Physiology, Georgia Health Sciences University, Augusta, GA, USA.
authors: R Clinton
authors: RC
authors: Webb
authors: Department of Pharmacology, Universidade Federal do Paraná, Curitiba, PR, Brazil; Laboratory of Cardiovascular Pharmacology, Department of Pharmacology, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil. Electronic address: j.e.silva.santos@ufsc.br.
authors: J Eduardo
authors: JE
authors: da Silva-Santos
mesh_terms: D000450:Aldosterone / Q000378:metabolism; D000803:Angiotensin I / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure; D019808:Losartan / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D012084:Renin-Angiotensin System; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D044140:Receptor, Angiotensin, Type 1; D017673:Sodium Chloride, Dietary; D000804:Angiotensin II; D000450:Aldosterone; D000803:Angiotensin I; D019808:Losartan
keywords: Angiotensin II receptors; Arterial pressure; High salt; Losartan; Vascular reactivity