Abstract

Blood flow regulation is a critical factor for tissue oxygenation and substrate supply. Increased reactivity of arteries to vasoconstrictors may increase vascular resistance, resulting in reduced blood flow. We aimed to investigate the effect of a high-fat (HF) diet on stiffness and vasoconstrictor reactivity of white adipose tissue (WAT) and brown adipose tissue (BAT) resistance arteries and also investigated the interconversion of both adipose depots in the setting of a HF diet. Vasoconstrictor reactivity and passive morphology and mechanical properties of arteries from B6D2F1 mice (5 mo old) fed normal chow (NC) or a HF diet (8 wk) were measured using pressure myography. Receptor gene expression in WAT and BAT arteries and markers of WAT and BAT were assessed in whole tissue lysates by real-time RT-PCR. Despite greater receptor-independent vasoconstriction (in response to KCl, P < 0.01), vasoconstriction in response to angiotensin II ( P < 0.01) was lower in NC-BAT than NC-WAT arteries and similar in response to endothelin-1 ( P = 0.07) and norepinephrine ( P = 0.11) in NC-BAT and NC-WAT arteries. With the exception of BAT artery reactivity to endothelin-1 and angiotensin II, the HF diet tended to attenuate reactivity in arteries from both adipose depots and increased expression of adipose markers in BAT. No significant differences in morphology or passive mechanical properties were found between adipose types or diet conditions. Alterations in gene expression of adipose markers after the HF diet suggest beiging of BAT. An increase in brown adipocytes in the absence of increased BAT mass may be a compensatory mechanism to dissipate excess energy from a HF diet. NEW & NOTEWORTHY Despite no differences in passive mechanical properties and greater receptor-independent vasoconstriction, receptor-mediated vasoconstriction was either lower in brown than white adipose tissue arteries or similar in brown and white adipose tissue arteries. A high-fat diet has a greater impact on vasoconstrictor responses in white adipose tissue but leads to altered adipose tissue gene expression consistent with beiging of the brown adipose tissue.

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