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Effect of perivascular adipose tissue on arterial adrenergic contractions in normotensive and hypertensive rats with high fructose intake
A. Zemančíková, J. Török
Language English Country Czech Republic
Document type Journal Article
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- MeSH
- Adrenergic Agents pharmacology MeSH
- Mesenteric Arteries drug effects physiology MeSH
- Fructose administration & dosage toxicity MeSH
- Hypertension physiopathology MeSH
- Blood Pressure drug effects physiology MeSH
- Rats MeSH
- Random Allocation MeSH
- Rats, Inbred SHR MeSH
- Rats, Inbred WKY MeSH
- Adipose Tissue blood supply drug effects physiology MeSH
- Vasoconstriction drug effects physiology MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
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.
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