Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension
Autor: | Scott A. Hahn, Pedro Lourenço Katayama, Leon J. DeLalio, Sean D. Stocker, Adam C. Straub, William B. Farquhar, Megan M. Wenner |
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Rok vydání: | 2020 |
Předmět: |
Male
medicine.medical_specialty aortic stiffness hypertension Physiology Blood Pressure Vasodilation 030204 cardiovascular system & hematology Renovascular hypertension Mice 03 medical and health sciences Vascular Stiffness 0302 clinical medicine Physiology (medical) Internal medicine medicine.artery salt sensitivity medicine Animals Sodium Chloride Dietary Pulse wave velocity Mesenteric arteries Aorta business.industry medicine.disease Pulse pressure Mice Inbred C57BL Hypertension Renovascular Endocrinology medicine.anatomical_structure Blood pressure Vasoconstriction Aortic stiffness Endothelium Vascular Cardiology and Cardiovascular Medicine business 2K1C 030217 neurology & neurosurgery Research Article |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology |
ISSN: | 1522-1539 0363-6135 |
Popis: | Renovascular hypertension is characterized by activation of the renin-angiotensin-aldosterone system, blunted natriuretic responses, and elevated sympathetic nerve activity. Excess dietary salt intake exaggerates arterial blood pressure (ABP) in multiple models of experimental hypertension. The present study tested whether a high-salt diet exaggerated ABP and vascular dysfunction in a 2-kidney, 1-clip (2K1C) murine model. Male C57BL/6J mice (8–12 wk) were randomly assigned, and fed a 0.1% or 4.0% NaCl diet, and instrumented with telemetry units to measure ABP. Then, the 2K1C model was produced by placing a cuff around the right renal artery. Systolic, diastolic, and mean ABP were significantly higher in mice fed 4.0% vs. 0.1% NaCl at 1 wk but not after 3 wk. Interestingly, 2K1C hypertension progressively increased arterial pulse pressure in both groups; however, the magnitude was significantly greater in mice fed 4.0% vs. 0.1% NaCl at 3 wk. Moreover, pulse wave velocity was significantly greater in 2K1C mice fed 4.0% vs. 0.1% NaCl diet or sham-operated mice fed either diet. Histological assessment of aortas indicated no structural differences among groups. Finally, endothelium-dependent vasodilation was significantly and selectively attenuated in the aorta but not mesenteric arteries of 2K1C mice fed 4.0% NaCl vs. 0.1% NaCl or sham-operated control mice. The findings suggest that dietary salt loading transiently exaggerates 2K1C renovascular hypertension but promotes chronic aortic stiffness and selective aortic vascular dysfunction. NEW & NOTEWORTHY High dietary salt exaggerates hypertension in multiple experimental models. Here we demonstrate that a high-salt diet produces a greater increase in arterial blood pressure at 1 wk after induction of 2-kidney, 1-clip (2K1C) hypertension but not at 3 wk. Interestingly, 2K1C mice fed a high-salt diet displayed an exaggerated pulse pressure, elevated pulse wave velocity, and reduced endothelium-dependent vasodilation of the aorta but not mesenteric arteries. These findings suggest that dietary salt may interact with underlying cardiovascular disease to promote selective vascular dysfunction and aortic stiffness. |
Databáze: | OpenAIRE |
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