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- W2902018032 abstract "Abstract Objectives This study sought to determine whether salt‐induced ANG II suppression contributes to impaired CBF autoregulation. Methods Cerebral autoregulation was evaluated with LDF during graded reductions of blood pressure. Autoregulatory responses in rats fed HS (4% NaCl) diet vs LS (0.4% NaCl) diet were analyzed using linear regression analysis, model‐free analysis, and a mechanistic theoretical model of blood flow through cerebral arterioles. Results Autoregulation was intact in LS ‐fed animals as MAP was reduced via graded hemorrhage to approximately 50 mm Hg. Short‐term (3 days) and chronic (4 weeks) HS diet impaired CBF autoregulation, as evidenced by progressive reductions of laser Doppler flux with arterial pressure reduction. Chronic low dose ANG II infusion (5 mg/kg/min, i.v.) restored CBF autoregulation between the pre‐hemorrhage MAP and 50 mm Hg in rats fed short‐term HS diet. Mechanistic‐based model analysis showed a reduced myogenic response and reduced baseline VSM tone with short‐term HS diet, which was restored by ANG II infusion. Conclusions Short‐term and chronic HS diet lead to impaired autoregulation in the cerebral circulation, with salt‐induced ANG II suppression as a major factor in the initiation of impaired CBF regulation." @default.
- W2902018032 created "2018-12-11" @default.
- W2902018032 creator A5030156095 @default.
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- W2902018032 creator A5064125344 @default.
- W2902018032 creator A5075058971 @default.
- W2902018032 creator A5076010626 @default.
- W2902018032 date "2019-01-15" @default.
- W2902018032 modified "2023-10-17" @default.
- W2902018032 title "High salt diet impairs cerebral blood flow regulation via salt‐induced angiotensin<scp>II</scp>suppression" @default.
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- W2902018032 doi "https://doi.org/10.1111/micc.12518" @default.
- W2902018032 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6465152" @default.
- W2902018032 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30481399" @default.
- W2902018032 hasPublicationYear "2019" @default.
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