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Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension.

Mikolajczyk TP, Nosalski R, Szczepaniak P, Budzyn K, Osmenda G, Skiba D, Sagan A, Wu J, Vinh A, Marvar PJ, Guzik B, Podolec J, Drummond G, Lob HE, Harrison DG, Guzik TJ - FASEB J. (2016)

Bottom Line: IFN-γ ex vivo caused significant endothelial dysfunction, which was reduced by superoxide anion scavenging.E., Harrison, D.G., Guzik, T.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Jagiellonian University, Cracow, Poland British Heart Foundation Centre for Excellence, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.

No MeSH data available.


Related in: MedlinePlus

RANTES in Ang II–dependent hypertension and regulation of vascular dysfunction in animal model and in humans. A) Effect of Ang II–induced hypertension on endothelium-dependent vasodilatation to ACh in aortas of WT and RANTES−/− mice (n = 6 for each). B) Relaxations to sodium nitroprusside as measure of non-endothelium-dependent vasodilatation (n = 6 for each). Statistical analysis was performed by repeated measures ANOVA. C) Aortic superoxide levels measured by monitoring oxidation of dihydroethidium to 2-hydroxyethidium using HPLC in WT and RANTES−/− mice infused for 14 d with buffer (sham) or Ang II (n = 5 each group). D) Mean daily values of invasive telemetric measurements of systolic (top left), diastolic (bottom left ), and mean arterial (top right) blood pressure and heart rate (bottom right) at baseline and during Ang II infusion in WT and RANTES−/− mice (n = 6). E) Correlation between serum RANTES levels and FMD in high-cardiovascular-risk cohort of 129 subjects. F) Relationship between RANTES serum levels and non-endothelium-dependent nitroglycerin-mediated dilatation induced vasodilatation this cohort. G) Relationship between RANTES and vWF (as biochemical marker for endothelial dysfunction) levels in serum of high-cardiovascular-risk cohort. E–G) Statistics for these relationships presented as Spearman’s correlation tests.
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Figure 3: RANTES in Ang II–dependent hypertension and regulation of vascular dysfunction in animal model and in humans. A) Effect of Ang II–induced hypertension on endothelium-dependent vasodilatation to ACh in aortas of WT and RANTES−/− mice (n = 6 for each). B) Relaxations to sodium nitroprusside as measure of non-endothelium-dependent vasodilatation (n = 6 for each). Statistical analysis was performed by repeated measures ANOVA. C) Aortic superoxide levels measured by monitoring oxidation of dihydroethidium to 2-hydroxyethidium using HPLC in WT and RANTES−/− mice infused for 14 d with buffer (sham) or Ang II (n = 5 each group). D) Mean daily values of invasive telemetric measurements of systolic (top left), diastolic (bottom left ), and mean arterial (top right) blood pressure and heart rate (bottom right) at baseline and during Ang II infusion in WT and RANTES−/− mice (n = 6). E) Correlation between serum RANTES levels and FMD in high-cardiovascular-risk cohort of 129 subjects. F) Relationship between RANTES serum levels and non-endothelium-dependent nitroglycerin-mediated dilatation induced vasodilatation this cohort. G) Relationship between RANTES and vWF (as biochemical marker for endothelial dysfunction) levels in serum of high-cardiovascular-risk cohort. E–G) Statistics for these relationships presented as Spearman’s correlation tests.

Mentions: RANTES shows significant functional effects in the vasculature, as the vasodilatation evoked by ACh was impaired in WT mice but not in RANTES−/− mice that had received Ang II (Fig. 3A). Endothelium-independent responses to sodium nitroprusside were not altered by Ang II in either WT or RANTES−/− mice (Fig. 3B). Vascular superoxide production did not differ between WT and RANTES−/− mice at baseline, but lack of RANTES was associated with abrogated Ang II–induced increase in vascular superoxide (Fig. 3C). We next examined the hypertensive response to Ang II in mice lacking RANTES using radiotelemetry (Fig. 3D). Ang II induced approximately equivalent degrees of hypertension in WT and RANTES−/− mice (Fig. 3D). Ang II-induced hypertension was associated with increased sensitivity to noradrenaline induced vasoconstriction and this effect was were unaltered in RANTES−/− mice (Supplemental Fig. S3)


Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension.

Mikolajczyk TP, Nosalski R, Szczepaniak P, Budzyn K, Osmenda G, Skiba D, Sagan A, Wu J, Vinh A, Marvar PJ, Guzik B, Podolec J, Drummond G, Lob HE, Harrison DG, Guzik TJ - FASEB J. (2016)

RANTES in Ang II–dependent hypertension and regulation of vascular dysfunction in animal model and in humans. A) Effect of Ang II–induced hypertension on endothelium-dependent vasodilatation to ACh in aortas of WT and RANTES−/− mice (n = 6 for each). B) Relaxations to sodium nitroprusside as measure of non-endothelium-dependent vasodilatation (n = 6 for each). Statistical analysis was performed by repeated measures ANOVA. C) Aortic superoxide levels measured by monitoring oxidation of dihydroethidium to 2-hydroxyethidium using HPLC in WT and RANTES−/− mice infused for 14 d with buffer (sham) or Ang II (n = 5 each group). D) Mean daily values of invasive telemetric measurements of systolic (top left), diastolic (bottom left ), and mean arterial (top right) blood pressure and heart rate (bottom right) at baseline and during Ang II infusion in WT and RANTES−/− mice (n = 6). E) Correlation between serum RANTES levels and FMD in high-cardiovascular-risk cohort of 129 subjects. F) Relationship between RANTES serum levels and non-endothelium-dependent nitroglycerin-mediated dilatation induced vasodilatation this cohort. G) Relationship between RANTES and vWF (as biochemical marker for endothelial dysfunction) levels in serum of high-cardiovascular-risk cohort. E–G) Statistics for these relationships presented as Spearman’s correlation tests.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4836375&req=5

Figure 3: RANTES in Ang II–dependent hypertension and regulation of vascular dysfunction in animal model and in humans. A) Effect of Ang II–induced hypertension on endothelium-dependent vasodilatation to ACh in aortas of WT and RANTES−/− mice (n = 6 for each). B) Relaxations to sodium nitroprusside as measure of non-endothelium-dependent vasodilatation (n = 6 for each). Statistical analysis was performed by repeated measures ANOVA. C) Aortic superoxide levels measured by monitoring oxidation of dihydroethidium to 2-hydroxyethidium using HPLC in WT and RANTES−/− mice infused for 14 d with buffer (sham) or Ang II (n = 5 each group). D) Mean daily values of invasive telemetric measurements of systolic (top left), diastolic (bottom left ), and mean arterial (top right) blood pressure and heart rate (bottom right) at baseline and during Ang II infusion in WT and RANTES−/− mice (n = 6). E) Correlation between serum RANTES levels and FMD in high-cardiovascular-risk cohort of 129 subjects. F) Relationship between RANTES serum levels and non-endothelium-dependent nitroglycerin-mediated dilatation induced vasodilatation this cohort. G) Relationship between RANTES and vWF (as biochemical marker for endothelial dysfunction) levels in serum of high-cardiovascular-risk cohort. E–G) Statistics for these relationships presented as Spearman’s correlation tests.
Mentions: RANTES shows significant functional effects in the vasculature, as the vasodilatation evoked by ACh was impaired in WT mice but not in RANTES−/− mice that had received Ang II (Fig. 3A). Endothelium-independent responses to sodium nitroprusside were not altered by Ang II in either WT or RANTES−/− mice (Fig. 3B). Vascular superoxide production did not differ between WT and RANTES−/− mice at baseline, but lack of RANTES was associated with abrogated Ang II–induced increase in vascular superoxide (Fig. 3C). We next examined the hypertensive response to Ang II in mice lacking RANTES using radiotelemetry (Fig. 3D). Ang II induced approximately equivalent degrees of hypertension in WT and RANTES−/− mice (Fig. 3D). Ang II-induced hypertension was associated with increased sensitivity to noradrenaline induced vasoconstriction and this effect was were unaltered in RANTES−/− mice (Supplemental Fig. S3)

Bottom Line: IFN-γ ex vivo caused significant endothelial dysfunction, which was reduced by superoxide anion scavenging.E., Harrison, D.G., Guzik, T.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Jagiellonian University, Cracow, Poland British Heart Foundation Centre for Excellence, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.

No MeSH data available.


Related in: MedlinePlus