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Hypertension impairs hypoxia-induced angiogenesis in men

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Garcia, VP, Rocha, HNM, Rocha, MP, Mattos, JD, Campos, MO, Mansur, DE, Secher, NH, Nóbrega, ACL, Fernandes, IA & Rocha, NG 2020, 'Hypertension impairs hypoxia-induced angiogenesis in men', Journal of Hypertension, vol. 38, no. 6, pp. 1131-1139. https://doi.org/10.1097/HJH.0000000000002369

APA

Garcia, V. P., Rocha, H. N. M., Rocha, M. P., Mattos, J. D., Campos, M. O., Mansur, D. E., Secher, N. H., Nóbrega, A. C. L., Fernandes, I. A., & Rocha, N. G. (2020). Hypertension impairs hypoxia-induced angiogenesis in men. Journal of Hypertension, 38(6), 1131-1139. https://doi.org/10.1097/HJH.0000000000002369

CBE

Garcia VP, Rocha HNM, Rocha MP, Mattos JD, Campos MO, Mansur DE, Secher NH, Nóbrega ACL, Fernandes IA, Rocha NG. 2020. Hypertension impairs hypoxia-induced angiogenesis in men. Journal of Hypertension. 38(6):1131-1139. https://doi.org/10.1097/HJH.0000000000002369

MLA

Vancouver

Garcia VP, Rocha HNM, Rocha MP, Mattos JD, Campos MO, Mansur DE et al. Hypertension impairs hypoxia-induced angiogenesis in men. Journal of Hypertension. 2020 Jun;38(6):1131-1139. https://doi.org/10.1097/HJH.0000000000002369

Author

Garcia, Vinicius P ; Rocha, Helena N M ; Rocha, Marcos P ; Mattos, João D ; Campos, Monique O ; Mansur, Daniel E ; Secher, Niels H ; Nóbrega, Antonio C L ; Fernandes, Igor A ; Rocha, Natália G. / Hypertension impairs hypoxia-induced angiogenesis in men. In: Journal of Hypertension. 2020 ; Vol. 38, No. 6. pp. 1131-1139.

Bibtex

@article{13f93d95f64e41fdaceb02c43cd29d3d,
title = "Hypertension impairs hypoxia-induced angiogenesis in men",
abstract = "OBJECTIVE: The inability of the organism to appropriately respond to hypoxia results in abnormal cell metabolism and function. Hypoxia-induced angiogenesis seems to be suppressed in experimental models of hypertension; however, this hypothesis has not been tested in humans. We examined changes in endothelial biomarkers and vascular chemoattraction/angiogenic capacity in response to isocapnic hypoxia in hypertensive men.METHODS: Twelve normotensive (38 ± 10 years) and nine hypertensive men (45 ± 11 years) were exposed to 5-min trials of normoxia (21% O2) and isocapnic hypoxia (10% O2). During the last minute of each trial, venous blood was drawn. Endothelial progenitor cells (EPCs; CD45/CD34/VEGFR2), endothelial microvesicles (apoptotic EMVs, CD42b/CD31/AnnexinV; endothelial activation, CD62E/CD144), nitrite, vascular endothelial growth factor (VEGF), and stromal cell-derived factor 1 (SDF-1) were measured.RESULTS: During normoxia, EPCs, nitrite, endothelial activation, and SDF-1 were similar between groups, whereas VEGF was lower (P = 0.02) and apoptotic EMVs tended to increase (P = 0.07) in hypertensive men. During isocapnic hypoxia, endothelial activation increased in both groups (normotensive, P = 0.007 vs. normoxia; hypertensive, P = 0.006 vs. normoxia), whereas EMVs were higher only in the hypertensive group (P = 0.03 vs. normotensive). EPCs (P = 0.01 vs. normoxia; P = 0.03 vs. hypertensive men), NO (P = 0.01 vs. normoxia; P = 0.04 vs. hypertensive), and VEGF (P = 0.02 vs. normoxia; P = 0.0005 vs. hypertensive) increased only in normotensive individuals in response to isocapnic hypoxia. SDF-1 did not change in either group.CONCLUSION: These results suggest that hypertension-induced impairment in angiogenesis in response to isocapnic hypoxia is related to disrupted NO bioavailability, VEGF chemotactic signaling, and EPC mobilization.",
author = "Garcia, {Vinicius P} and Rocha, {Helena N M} and Rocha, {Marcos P} and Mattos, {Jo{\~a}o D} and Campos, {Monique O} and Mansur, {Daniel E} and Secher, {Niels H} and N{\'o}brega, {Antonio C L} and Fernandes, {Igor A} and Rocha, {Nat{\'a}lia G}",
year = "2020",
month = jun,
doi = "10.1097/HJH.0000000000002369",
language = "English",
volume = "38",
pages = "1131--1139",
journal = "Journal of Hypertension",
issn = "0263-6352",
publisher = "Lippincott Williams & Wilkins, Ltd",
number = "6",

}

RIS

TY - JOUR

T1 - Hypertension impairs hypoxia-induced angiogenesis in men

AU - Garcia, Vinicius P

AU - Rocha, Helena N M

AU - Rocha, Marcos P

AU - Mattos, João D

AU - Campos, Monique O

AU - Mansur, Daniel E

AU - Secher, Niels H

AU - Nóbrega, Antonio C L

AU - Fernandes, Igor A

AU - Rocha, Natália G

PY - 2020/6

Y1 - 2020/6

N2 - OBJECTIVE: The inability of the organism to appropriately respond to hypoxia results in abnormal cell metabolism and function. Hypoxia-induced angiogenesis seems to be suppressed in experimental models of hypertension; however, this hypothesis has not been tested in humans. We examined changes in endothelial biomarkers and vascular chemoattraction/angiogenic capacity in response to isocapnic hypoxia in hypertensive men.METHODS: Twelve normotensive (38 ± 10 years) and nine hypertensive men (45 ± 11 years) were exposed to 5-min trials of normoxia (21% O2) and isocapnic hypoxia (10% O2). During the last minute of each trial, venous blood was drawn. Endothelial progenitor cells (EPCs; CD45/CD34/VEGFR2), endothelial microvesicles (apoptotic EMVs, CD42b/CD31/AnnexinV; endothelial activation, CD62E/CD144), nitrite, vascular endothelial growth factor (VEGF), and stromal cell-derived factor 1 (SDF-1) were measured.RESULTS: During normoxia, EPCs, nitrite, endothelial activation, and SDF-1 were similar between groups, whereas VEGF was lower (P = 0.02) and apoptotic EMVs tended to increase (P = 0.07) in hypertensive men. During isocapnic hypoxia, endothelial activation increased in both groups (normotensive, P = 0.007 vs. normoxia; hypertensive, P = 0.006 vs. normoxia), whereas EMVs were higher only in the hypertensive group (P = 0.03 vs. normotensive). EPCs (P = 0.01 vs. normoxia; P = 0.03 vs. hypertensive men), NO (P = 0.01 vs. normoxia; P = 0.04 vs. hypertensive), and VEGF (P = 0.02 vs. normoxia; P = 0.0005 vs. hypertensive) increased only in normotensive individuals in response to isocapnic hypoxia. SDF-1 did not change in either group.CONCLUSION: These results suggest that hypertension-induced impairment in angiogenesis in response to isocapnic hypoxia is related to disrupted NO bioavailability, VEGF chemotactic signaling, and EPC mobilization.

AB - OBJECTIVE: The inability of the organism to appropriately respond to hypoxia results in abnormal cell metabolism and function. Hypoxia-induced angiogenesis seems to be suppressed in experimental models of hypertension; however, this hypothesis has not been tested in humans. We examined changes in endothelial biomarkers and vascular chemoattraction/angiogenic capacity in response to isocapnic hypoxia in hypertensive men.METHODS: Twelve normotensive (38 ± 10 years) and nine hypertensive men (45 ± 11 years) were exposed to 5-min trials of normoxia (21% O2) and isocapnic hypoxia (10% O2). During the last minute of each trial, venous blood was drawn. Endothelial progenitor cells (EPCs; CD45/CD34/VEGFR2), endothelial microvesicles (apoptotic EMVs, CD42b/CD31/AnnexinV; endothelial activation, CD62E/CD144), nitrite, vascular endothelial growth factor (VEGF), and stromal cell-derived factor 1 (SDF-1) were measured.RESULTS: During normoxia, EPCs, nitrite, endothelial activation, and SDF-1 were similar between groups, whereas VEGF was lower (P = 0.02) and apoptotic EMVs tended to increase (P = 0.07) in hypertensive men. During isocapnic hypoxia, endothelial activation increased in both groups (normotensive, P = 0.007 vs. normoxia; hypertensive, P = 0.006 vs. normoxia), whereas EMVs were higher only in the hypertensive group (P = 0.03 vs. normotensive). EPCs (P = 0.01 vs. normoxia; P = 0.03 vs. hypertensive men), NO (P = 0.01 vs. normoxia; P = 0.04 vs. hypertensive), and VEGF (P = 0.02 vs. normoxia; P = 0.0005 vs. hypertensive) increased only in normotensive individuals in response to isocapnic hypoxia. SDF-1 did not change in either group.CONCLUSION: These results suggest that hypertension-induced impairment in angiogenesis in response to isocapnic hypoxia is related to disrupted NO bioavailability, VEGF chemotactic signaling, and EPC mobilization.

U2 - 10.1097/HJH.0000000000002369

DO - 10.1097/HJH.0000000000002369

M3 - Journal article

C2 - 32371803

VL - 38

SP - 1131

EP - 1139

JO - Journal of Hypertension

JF - Journal of Hypertension

SN - 0263-6352

IS - 6

ER -

ID: 62408684