Key result
High-fructose, high-salt diet increases aortic PWV ~29% in male rats, reversible by sympathoinhibition.
Why the study?
To evaluate whether activation of the renin-angiotensin system and/or the sympathetic system mediates aortic stiffness in rats with fructose-induced salt-sensitive blood pressure.
Does acute sympathoinhibition or RAS inhibition improve aortic stiffness in rats with fructose-induced salt-sensitive blood pressure?
Does acute sympathoinhibition or RAS inhibition improve aortic stiffness in rats with fructose-induced salt-sensitive blood pressure?
Absolute Event Rate: 793% vs 616%
p-value: p=<0.001
Adult female rats are protected from fructose and high salt diet-induced blood pressure increases and aortic stiffness, whereas affected male rats show improved aortic compliance with acute sympathoinhibition.
Sex-specific aortic stiffness from fructose-salt diet in rats is hypothesis-generating; leaves open human relevance and sympathoinhibition translation.
Hypertension is the leading risk factor for major adverse cardiovascular events (MACE). Aortic stiffness and sympathoexcitation are robust predictors of MACE. Combined high fructose and sodium intake increases arterial pressure, aortic stiffness, renin, and sympathetic nerve activity in male rats. We hypothesized that activation of the renin angiotensin system (RAS) and/or the sympathetic system mediates aortic stiffness in rats with fructose-induced salt-sensitive blood pressure. Male and female Sprague-Dawley rats ingested 20% fructose or 20% glucose in drinking water with 0.4% NaCl chow for 1 week. Then, fructose-fed rats were switched to 4% NaCl chow (Fru + HS); glucose-fed rats remained on 0.4% NaCl chow (Glu + NS, controls for caloric intake). After 2 weeks, mean arterial pressure (MAP) and aortic pulsed wave velocity (PWV) were evaluated at baseline or after acute intravenous vehicle, clonidine, enalapril, losartan, or hydrochlorothiazide. Baseline global longitudinal strain (GLS) was also assessed. MAP and PWV were greater in male Fru + HS versus Glu + NS male rats (p < 0.05 and p < 0.001, respectively). PWV was similar between the female groups. Despite similarly reduced MAP after clonidine, PWV decreased in Fru + HS versus Glu + NS male rats (p < 0.01). Clonidine induced similar decreases in MAP and PWV in females on either diet. GLS was lower in Fru + HS versus Glu + NS male rats and either of the female groups. Thus, acute sympathoinhibition improved aortic compliance in male rats with fructose salt-sensitive blood pressure. Female rats retained aortic compliance regardless of diet. Acute RAS inhibition exerted no significant effects. Male rats on fructose high salt diet displayed an early deficit in myocardial function. Taken together, these findings suggest that adult female rats are protected from the impact of fructose and high salt diet on blood pressure, aortic stiffness, and early left ventricular dysfunction compared with male rats.
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Komnenov et al. (2023) studied Fructose-induced salt-sensitive hypertension and aortic stiffness (n=34). High-fructose and high-salt diet vs. 20% glucose in water and 0.4% NaCl chow was evaluated on Aortic pulse wave velocity (PWV) in male rats (p=<0.001). A high-fructose, high-salt diet significantly increased aortic pulse wave velocity in male rats compared to controls (793 vs 616 mm/s), an effect reversed by acute sympathoinhibition, whereas female rats were protected.
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