Role of Ang AT1a receptors in the ACE and cardiovascular responses to a fructose diet

Abstract

A high fructose diet is associated with cardiovascular dysfunction which may be related to activation of the renin angiotensin system. The aim was to test a high fructose diet in mice lacking Ang AT1a receptors, measuring the changes in mean arterial pressure (MAP) and ACE activity. AT1a knockout (KO‐C) and wild type (WT‐C) mice were fed a standard diet (Control). AT1a knockout (KO‐F) and wild type (WT‐F) mice were fed a fructose diet (60% fructose). Blood pressure recordings were made at week 8 and blood was collected. ACE activity was determined in plasma (1 ìL) using a mass spectroscopic (MS) based proteolytic assay. Fructose increased MAP in WT‐F (8% increase vs. WT‐C). Plasma ACE activity was increased in WT‐F as compared to the other groups (1.4±0.3; 0.8±0.1; 0.6±0.06; 0.5±0.06 Ang II/Ang I; WT‐F, WT‐C, KO‐F, KO‐C, respectively). The fructose diet decreased MAP in the KO (24% decrease vs. KO‐C). In the presence of an intact Ang AT1a receptor system, fructose increased ACE and MAP. In the gene deletion model, there was hypotension with no changes in ACE. Results document important interactions between the genetics and diet with an association between plasma ACE and blood pressure.