TY - JOUR
T1 - Enhanced angiotensin-converting enzyme activity and systemic reactivity to angiotensin II in normotensive rats exposed to a high-sodium diet
AU - Crestani, Sandra
AU - Gasparotto Júnior, Arquimedes
AU - Marques, Maria C.A.
AU - Sullivan, Jennifer C.
AU - Webb, R. Clinton
AU - Da Silva-Santos, J. Eduardo
N1 - Funding Information:
We thank Nuvital Nutrientes SA (Colombo, PR, Brazil) for the donation of chow used in the preliminary experiments. This work was supported, in part, by grants from the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, Brazil, 482214/2007-4 ), and from the National Heart, Lung, and Blood Institute (USA, R01HL071138 ). Sandra Crestani received a PhD fellowship from Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES, Brazil).
PY - 2014/2
Y1 - 2014/2
N2 - 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.
AB - 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.
KW - Angiotensin II receptors
KW - Arterial pressure
KW - High salt
KW - Losartan
KW - Vascular reactivity
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U2 - 10.1016/j.vph.2013.12.001
DO - 10.1016/j.vph.2013.12.001
M3 - Article
C2 - 24321189
AN - SCOPUS:84893802958
SN - 1537-1891
VL - 60
SP - 67
EP - 74
JO - Vascular Pharmacology
JF - Vascular Pharmacology
IS - 2
ER -