Effect of Perivascular Adipose Tissue on Arterial Adrenergic Contractions in Normotensive and Hypertensive Rats With High Fructose Intake

Abstract

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 pro-hypertensive 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.

Fructose Intake Impairs the Synergistic Vasomotor Manifestation of Nitric Oxide and Hydrogen Sulfide in Rat Aorta

“…In our study, we confirmed that the long-lasting increase in fructose treatment did not affect the maximal force of adrenergic contraction but increased the sensitivity of adrenergic receptors to exogenous noradrenaline and significantly reduced endothelium-dependent vasorelaxation, although did not alter relaxation to NO donors (Figure 3a-d). Similar findings were observed by Zemancikova et al (2014) [7], who reported an unchanged adrenergic contraction but decreased acetylcholine-induced vasorelaxation in the thoracic aorta of normotensive Wistar rats drinking 10% fructose solution. Moreover, they pointed out that fructose did not induce cardiovascular alterations in rats without a functional NO system in the state of NO deficiency (induced by N G -nitro-L-arginine methylester (LN) administration).…”

“…However, according to other available studies, the question of a direct association of high fructose consumption with an increase in blood pressure represents a controversial issue. Chronic fructose administration significantly elevated SBP in normotensive conditions [ 1 , 7 , 15 ]; on the other hand, some authors found no impact of this treatment on blood pressure [ 16 , 17 ]. In our study, although we revealed a significant effect of the eight-week fructose administration on the values of systolic blood pressure, there were no differences between the experimental groups in individual weeks ( Figure 1 ).…”

“…Animals chronically receiving high amounts of fructose developed hypertriglyceridemia, insulin resistance, hyperinsulinemia, and often obesity and hypertension [ 4 , 5 , 6 ]. Zemancikova and Torok (2014) [ 7 ] also reported that eight weeks of fructose administration to adult Wistar rats induced metabolic changes associated with an increase in plasma glucose and lipids, enlargement of the liver, significant blood pressure elevation, and reduction in endothelium-derived vasorelaxation. The authors also pointed out the specific role of NO/NOS signaling in these processes, because simultaneous treatment with a NOS inhibitor and fructose did not evoke the abovementioned pathological changes.…”

Influence of Age on Anticontractile Effect of Perivascular Adipose Tissue in Normotensive and Hypertensive Rats

“…However, concerning the differences in PVAT between SHR and WKY rats, qualitative distinctions seem to be more important than the quantitative ones [29]. To support this concept, in our previous study, we have demonstrated that moderate increase in body adiposity potentiates the anticontractile effect of PVAT in normotensive WKY rats but not in SHR [15]. Therefore, it is evident that SHR have qualitatively different PVAT, and the increase in amount of this tissue might not cause its larger anticontractile effect.…”

“…On the other hand, the impairment in anticontractile action of mesenteric arterial PVAT was detected also in spontaneously hypertensive rats (SHR), which are characteristic by lower body weight comparing to normotensive Wistar-Kyoto rats [12], and this defect in PVAT was shown to be associated with the exaggerated sensitivity of SHR arteries to vasoconstrictors [13, 14]. Moderate growth in adipose mass due to high fructose intake potentiated the anticontractile properties of PVAT in normotensive rats but it did not improve them in SHR, indicating that qualitative rather than quantitative changes of PVAT are important when considering its participation in increased vascular tone in SHR [15].…”