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Long Term Hypoxia Reduces Ca 2+ Oscillations in Basilar Arterial Myocytes of Fetal and Adult Sheep
Author(s) -
Reid Casey,
Romero Monica,
Dobyns Abigail,
Wilson Christopher G.,
Hessinger David A.,
Longo Lawrence D.,
Zhang Lubo,
Wilson Sean M.
Publication year - 2018
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.2018.32.1_supplement.858.9
Subject(s) - vasoconstriction , fetus , cerebral arteries , medicine , hypoxia (environmental) , biology , endocrinology , cerebral circulation , depolarization , neuroscience , chemistry , oxygen , pregnancy , organic chemistry , genetics
Ca 2+ oscillations are important in the regulation of many cerebral arterial functions ranging from vasoconstriction to gene transcription. Without these oscillatory waveforms, there are alterations in the signaling pathways regulated by Ca 2+ . Previous work has shown that long term hypoxia (LTH) due to high altitude exposure can cause cerebral vascular dysfunction including changes in reactivity and morphology in the fetus as well as adult. Studies performed in cerebral arterial preparations have illustrated that LTH in sheep fetus and adult cause whole cell Ca 2+ signaling dysfunctions that compromise vascular reactivity and contribute to cerebral arterial pathologies. Based on the premise that Ca 2+ oscillations, vasoconstriction, vessel morphology, and LTH mediated cerebral arterial function are interrelated we tested the hypothesis that LTH impairs Ca 2+ oscillations. The impact of LTH and maturation on Ca 2+ signals in cerebral arterial myocytes was examined using confocal imaging techniques of flou‐4 loaded myocytes of basilar arteries from low (700m) or high altitude (3,801m) near term fetal or adult sheep. LTH decreased the intracellular Ca 2+ signals independent of age due to a faster decay in the Ca 2+ signal, an effect that could impair vasoconstriction, alter tissue structure, and compromise the regulation of cerebral blood flow. Along with producing smaller Ca 2+ events, the data show that LTH inhibits the cell's ability to respond with Ca 2+ signals in response to 30 mM potassium‐induced depolarization in fetal as well as adult sheep. LTH and ontogeny may also play interconnected roles in Ca 2+ signaling as LTH inhibits distant communication between myocytes in fetal sheep, whereas in adult sheep it stimulates local signaling. These observations illustrate that altitude and maturation each modify Ca 2+ signaling behavior in ways that likely impact arterial reactivity and other mechanisms related to the regulation of cerebral blood flow. Support or Funding Information This work is supported by The National Institutes of Health, Eunice Kennedy Shriver National Institute of Child Health and Human Development grant number HD083132, by the National Science Foundation under Grant No. MRI 0923559, and the Loma Linda University School of Medicine. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .