OBJECTIVES: High-salt diet likely elevates blood pressure (BP), thus increasing the risk of cardiovascular events. We hypothesized that a high-salt diet plays a critical role in subjects whose renin-angiotensin systems cannot adjust to variable salt intake, rendering them more susceptible to atherosclerosis. METHODS: Apolipoprotein E-deficient (ApoE-/-) mice received standard or high-salt diet (8%) alone or in combination with fixed angiotensin II (Ang II) infusion (0.5 microg/kg per min). BP was measured using telemetry, and plaque burden was assessed in the thoracic aorta and innominate artery. We used urinary isoprostane as a marker for oxidative stress. RESULTS: Although high-salt diet per se did not affect plaque extension, high salt combined with Ang II increased plaque area significantly in both the aorta and the innominate artery as compared with Ang II or salt alone (P < 0.05 and P < 0.01, respectively). High-salt diet did not affect BP or isoprostane levels, whereas Ang II infusion increased both BP and isoprostane levels (P < 0.05 and P < 0.01, respectively). Although high-salt diet combined with Ang II did not amplify BP, salt in combination with Ang II increased isoprostane levels further (P < 0.001 vs. Ang II alone). Ang II increases macrophage content in lesions (P < 0.05), whereas salt likely increases collagen content. CONCLUSION: High-salt diet per se does not influence BP in ApoE-/- mice and is only moderately atherogenic. Possibly mediated via increased oxidative stress, a high-salt diet combined with fixed high Ang II levels accelerates atherogenesis synergistically, beyond the effect of BP.
OBJECTIVES: High-salt diet likely elevates blood pressure (BP), thus increasing the risk of cardiovascular events. We hypothesized that a high-salt diet plays a critical role in subjects whose renin-angiotensin systems cannot adjust to variable salt intake, rendering them more susceptible to atherosclerosis. METHODS: Apolipoprotein E-deficient (ApoE-/-) mice received standard or high-salt diet (8%) alone or in combination with fixed angiotensin II (Ang II) infusion (0.5 microg/kg per min). BP was measured using telemetry, and plaque burden was assessed in the thoracic aorta and innominate artery. We used urinary isoprostane as a marker for oxidative stress. RESULTS: Although high-salt diet per se did not affect plaque extension, high salt combined with Ang II increased plaque area significantly in both the aorta and the innominate artery as compared with Ang II or salt alone (P < 0.05 and P < 0.01, respectively). High-salt diet did not affect BP or isoprostane levels, whereas Ang II infusion increased both BP and isoprostane levels (P < 0.05 and P < 0.01, respectively). Although high-salt diet combined with Ang II did not amplify BP, salt in combination with Ang II increased isoprostane levels further (P < 0.001 vs. Ang II alone). Ang II increases macrophage content in lesions (P < 0.05), whereas salt likely increases collagen content. CONCLUSION: High-salt diet per se does not influence BP in ApoE-/- mice and is only moderately atherogenic. Possibly mediated via increased oxidative stress, a high-salt diet combined with fixed high Ang II levels accelerates atherogenesis synergistically, beyond the effect of BP.
Authors: Hong Lu; Congqing Wu; Deborah A Howatt; Anju Balakrishnan; Richard J Charnigo; Lisa A Cassis; Alan Daugherty Journal: J Nutr Biochem Date: 2012-06-15 Impact factor: 6.048
Authors: Marcus A Ulleryd; Evelina Bernberg; Li Jin Yang; Göran M L Bergström; Maria E Johansson Journal: Biomed Res Int Date: 2014-07-08 Impact factor: 3.411