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Preservation of Ca 2+ spark activity during oxidative stress in pulmonary arterial myocytes of fetal sheep (1089.5)
Author(s) -
Suarez Gema,
Glasgow Shane,
Romero Monica,
Osman Noah,
Puglisi Jose,
Bers Donald,
Izu Leighton,
Longo Lawerence,
Wilson Sean
Publication year - 2014
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.28.1_supplement.1089.5
Subject(s) - oxidative stress , hypoxia (environmental) , fetus , vasodilation , reactive oxygen species , chemistry , medicine , pulmonary hypertension , antioxidant , oxidative phosphorylation , endocrinology , cardiology , oxygen , biology , biochemistry , pregnancy , organic chemistry , genetics
Antenatal chronic hypoxia can lead to pulmonary hypertension in newborns or more severe vascular remodeling and dangerous elevations in pressure. We have previously shown that antenatal chronic hypoxia deregulates Ca 2+ spark activity, which are important to pulmonary vasodilation at birth. Chronic hypoxia can also increase oxidative stress, which can impair Ca 2+ spark activity. In this research, we examined the impact of oxidative stress on Ca 2+ spark activity, which other laboratories have shown to increase Ca 2+ spark activity. We exposed pulmonary arteries from normoxic fetal sheep to reactive oxygen species (ROS) to mimic oxidative stress such as might occur with acute hypoxic stress by treating them with tert‐butyl H 2 O 2 and reduced ROS with the antioxidant N‐Acetyl‐L‐Cysteine (NAC). Using customized analysis software, roughly 7 % of control cells had Ca 2+ sparks and the frequency was 0.07 sparks/100 μm/sec. Spark activity was maintained in the presence of tert‐butyl H 2 O 2 and NAC. The spatial and temporal aspects to the Ca 2+ sparks were then determined. Spark amplitudes were unaffected as was the width. However, Ca 2+ spark decay was increased slightly by tert‐butyl H 2 O 2 . Overall, oxidative stress has only a mild influence on Ca 2+ spark activity on fetal pulmonary arteries from normoxic sheep. Grant Funding Source : Supported by NSF MRI 923559, NIH HD69746, P01HD31226, R01HD3807, LLUSOM, APS Frontiers in Physiology