Key result
High fructose intake for eight weeks in normotensive rats significantly reduced arterial adrenergic contractions (AUC 3.27 vs 6.09, p<0.001) by enhancing the anticontractile action of perivascular adipose tissue, an effect absent in hypertensive rats.
Why the study?
Does high fructose intake alter arterial adrenergic contractions and their modulation by perivascular adipose tissue in normotensive and hypertensive rats?
Does high fructose intake alter arterial adrenergic contractions and their modulation by perivascular adipose tissue in normotensive and hypertensive rats?
Absolute Event Rate: 3.27% vs 6.09%
p-value: p=<0.001
Moderate adiposity increase from fructose overfeeding enhances the anticontractile effect of perivascular adipose tissue in normotensive rats, but this protective mechanism is absent in spontaneously hypertensive rats.
Does not inform human dietary advice; leaves open perivascular mechanisms for translational research.
The aim of this study was to investigate the effect of high fructose intake associated with moderate increase in adiposity on rat arterial adrenergic responses and their modulation by perivascular adipose tissue (PVAT). After eight-week-lasting substitution of drinking water with 10 % fructose solution in adult normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), their systolic blood pressure, plasma triglycerides, and relative liver weight were elevated when compared to their respective control groups. Moreover, in SHR, body weight and relative heart weight were increased after treatment with fructose. In superior mesenteric arteries, PVAT exerted inhibitory influence on adrenergic contractile responses and this effect was markedly stronger in control WKY than in SHR. In fructose-administered WKY, arterial adrenergic contractions were substantially reduced in comparison with the control group; this was caused mainly by enhancement of anticontractile action of PVAT. The diminution of the mesenteric arterial contractions was not observed after fructose treatment in SHR. We conclude that the increase in body adiposity due to fructose overfeeding in rats might have prehypertensive effect. However, in WKY it might cause PVAT-dependent and independent reduction in arterial contractile responses to adrenergic stimuli, which could attenuate the pathological elevation in vascular tone.
No takes yet. Share an insight, caveat, or question.
Zemančíková et al. (2017) studied Hypertension and fructose-induced adiposity (n=33). High fructose intake vs. Tap water was evaluated on Arterial adrenergic contractions to exogenous noradrenaline (AUC) in PVAT-intact mesenteric arteries of normotensive rats (p=<0.001). High fructose intake for eight weeks in normotensive rats significantly reduced arterial adrenergic contractions (AUC 3.27 vs 6.09, p<0.001) by enhancing the anticontractile action of perivascular adipose tissue, an effect absent in hypertensive rats.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: