Anna Zemancikova's research while affiliated with Slovak Academy of Sciences and other places

... We found that in spontaneously hypertensive rats (SHRs), a model mimicking human essential hypertension, MLN induced detrimental effects on adiposity, the function of small arteries and angiogenesis, as well as a reduction in the ACE inhibitor (ACEI)induced hypotensive effect. However, in the thoracic aorta, compensatory mechanisms involving accentuation of NO and H 2 S signaling have been described, thus pointing to the complex action of ACE2 inhibitor [6]. ...

... The functional role of PVAT is unclear, but it depends on the type of vascular bed and the experimental species from which it is isolated [78]. A significant anticontractile effect in response to vasoconstrictors was demonstrated in various arteries, e.g., mesenteric resistance arteries, skeletal muscle arteries, thoracic aorta, etc. [87,88], and this effect is lost in obesity, probably as a consequence of the development of adipocyte hypertrophy, inflammation and oxidative stress [89]. Obesity, which enhances oxidative stress, worsens PVAT dysfunction and thus contributes to vascular damage [90]. ...

... [67][68][69] Besides, endothelial dysfunction decrease glutathione and endogenous antioxidant system activity as well as decreases releasing of hydrogen sulfide by endothelial cells. [70,71] The current advances in molecular biology have identified a group of interactions between lncRNAs, microRNAs (miRNAs or miRs), and the Ser/Thr kinase AKT that synergistically act to impair endothelial cell function. [72,73] In sustained hyperglycemic and uncontrolled glucose state, the lncRNA MIR181A2 is downregulated with reducing the ability to sponge miR68325p, miR68425p, and miR8056 which consequently leads to elevation of the miR68325p, miR68425p, and miR8056 concentration. ...

... The animals were distributed into 4 experimental groups: vehicle-treated Lean ZDF control ("Lean"; n = 8), QUE-treated Lean ZDF rats ("Lean + QUE"; n = 9), vehicle-treated Obese ZDF control ("Obese"; n = 13), and QUE-treated Obese ZDF rats ("Obese + QUE"; n = 14). QUE (#Q4951, ≥95% purity; Sigma-Aldrich, St. Louis, MO, USA) was dissolved in ethanol (Sigma-Aldrich, St. Louis, MO, USA) and provided in a biscuit (vehicle) at a concentration of 20 mg/kg/day for 6 weeks [75,76]. For the Lean and Obese controls, the biscuit contained a small amount of ethanol. ...

... L-nitro-arginine-methyl-ester (L-NAME), a NOS substrate, is used to inhibit NO synthesis and also associated with increased production of ROS and depletion of endogenous antioxidants (Vrankova et al., 2019). Such inhibition triggers an L-NAME increase in blood pressure, reduces the cyclic guanosine monophosphate (cGMP) levels of cardiac and aortic tissue (Veerappan and Malarvili, 2019), promotes intra-cellular signaling (including protein kinase C activity) in response to vasoactive agents such as angiotensin II, increases macrophage accumulation in perivascular areas and the arterial intima (the innermost vessel layers), and enhances oxidative stress by stimulating the expression of specific adhesion molecules (Gonzalez et al., 2000). ...

... In 2019, Pechanova et al. loaded the renin inhibitor aliskiren onto polylactic acid (PLA) polymeric NPs to study its effects on blood pressure, nitric oxide synthase activity in the heart, vasoactivity of the mesenteric artery and collagen accumulation in the heart of the SHR [118]. PLA NPs were prepared by the nanoprecipitation method. ...

... Recently we have shown that in the isolated superior MA, the presence of PVAT caused a reduction in contractions induced by exogenous as well as endogenous norepinephrine, while PVAT exerted no inhibitory effect on these responses in the abdominal aorta Zemancikova and Torok 2019). These differences can partially be related to the different distribution of the sympathetic innervation within the arterial wall and in PVAT . ...

... ZDF rats seemed to have higher sympathetic innervation together with enhanced sensitivity to noradrenergic stimulation in mesenteric arteries; however, their increased adrenergic responses were specifically blunted with PVAT anticontractile effect. On the contrary, Wistar rats had decreased adrenergic sensitivity and sparser innervation of mesenteric arterial smooth muscle; however, richer content of sympathetic nerve terminals in mesenteric PVAT might overlap its potential anticontractile effect, causing the adrenergic contractions being even higher in arteries with preserved PVAT, as described previously in abdominal aorta (44). ...

... We also demonstrated that chronic fructose intake impaired the synergistic vasomotor manifestation of nitric oxide (NO) and hydrogen sulfide (H 2 S) in these rats [2]. In spontaneously hypertensive rats (SHRs) fed with fructose, an increased level of triacylglycerols in plasma, an additional increase in systolic blood pressure, and kidney and heart hypertrophy were demonstrated; however, significant changes in vasoactive responses of the mesenteric artery were not observed [3]. ...

... This response was inhibited by PD98059, suggesting that ERK1/2 is involved in angiotensin II-induced vasoconstriction in SHRs 20) . It was also reported that ADRFs antagonize the contractile effect of noradrenaline in the mesenteric artery of WKY rats, but the effects are attenuated in SHRs 21) . These findings support the results of the present study. ...