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Altered Hypoxia‐Induced Vascular Reactivity and Endothelial Repair Capacity in Hypertensive Men
Author(s) -
Rocha Helely Miguens,
Garcia Vinicius Pacheco,
Mattos João Dario,
Rocha Marcos Paulo,
Campos Monique Opuszcka,
Jesus Mansur Daniel Elias,
Nóbrega Antonio Claudio Lucas,
Fernandes Igor Alexandre,
Rocha Natália Galito
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.709.2
Subject(s) - medicine , microneurography , hypoxia (environmental) , vasodilation , endothelial dysfunction , endothelium , endocrinology , nitric oxide , blood pressure , cardiology , anesthesia , chemistry , heart rate , baroreflex , organic chemistry , oxygen
Hypoxia induces peripheral vasodilation in healthy subjects, despite the occurrence of sympathoexcitation. Endothelial progenitor cells (EPC) mobilization from bone marrow and nitric oxide released by intact endothelium seem to exert important functions in the vasodilatory response to hypoxia. Even considering that both sympathetic overstimulation and endothelial dysfunction are major contributing factors to the pathophysiology of hypertension, it is still unknown whether those functions are preserved in patients with hypertension. Aim To determine the effects of hypoxia on sympathetic activity, peripheral blood flow, and endothelial biomarkers in patients with hypertension. Methods Six normotensive men (NT; 44 ± 11 yrs, mean arterial pressure (MAP) 87 ± 6 mmHg) and seven non‐treated patients with hypertension (HT; 44 ± 10 yrs, MAP 110 ± 7 mmHg) were exposed to 5‐min bouts of: (1) Normoxia (21% O 2 ) and (2) isocapnic‐Hypoxia (10% O 2 ). Muscle sympathetic nerve activity [MSNA (microneurography; peroneal nerve)] recordings were obtained throughout the protocol, while femoral artery blood flow measurements (Doppler ultrasound) and blood samples were acquired during the last 30s of each condition. EPC (CD45dim/CD34+/VEGFR2+) and endothelial microparticles (EMP; CD42b‐/CD31+/AnnexinV+) were measured by flow cytometry, whereas nitrite concentration was determined by ozone‐chemiluminescence method. Results At baseline, femoral arterial blood flow (HT 361.8 ± 262.6 ml.min −1 vs. NT 344.6 ± 75.5 ml.min −1 ), EMP (HT 12 ± 8 EMP/μL vs. NT 4 ± 1 EMP/μL) and nitrite (HT 0.35 ± 0.10 μM vs. NT 0.42 ± 0.12 μM) were similar between groups (p>0.05), while EPC were reduced in HT (35 ± 8 EPC/μL) compared to NT (86 ± 24 EPC/μL, p=0.02). During hypoxia, HT presented decreased femoral arterial blood flow (−110.2 ± 43.0 ml.min −1 ) and EPC (−7 ± 4 EPC/μL), while NT showed increased femoral arterial blood flow (+73.9 ± 37.4 ml.min −1 , p=0.01) and EPC (98 ± 35 EPC/μL, p=0.01). MSNA increased only in HT (+12.7 ± 6.7 vs. NT +3.6 ± 1.6 bursts/min, p=0.01). There were no differences in nitrite (HT −0.01 ± 0.07 μM vs. NT 0.06 ± 0.09 μM) and EMP (HT 6.4 ± 16.1 EMP/μL vs. NT 3.5 ± 3.9 EMP/μL) between groups (p>0.05). Conclusion These results suggest that patients with hypertension present diminished peripheral vascular reactivity in response to hypoxia, which could be associated with increased sympathetic activity observed in these individuals. Furthermore, EPC only increased in healthy subjects, suggesting an impaired endothelial repair capacity in patients with hypertension. Support or Funding Information CNPq, FAPERJ, CAPES and FINEP.