Long-term hypoxia modulates depolarization activation of BK currents in fetal sheep middle cerebral arterial myocytes.

Introduction: Previous evidence indicates that gestational hypoxia disrupts cerebrovascular development, increasing the risk of intracranial hemorrhage and stroke in the newborn. Due to the role of cytosolic Ca in regulating vascular smooth muscle (VSM) tone and fetal cerebrovascular blood flow, understanding Ca signals can offer insight into the pathophysiological disruptions taking place in hypoxia-related perinatal cerebrovascular disease. This study aimed to determine the extent to which gestational hypoxia disrupts local Ca sparks and whole-cell Ca signals and coupling with BK channel activity.

Improved Workflow for Analysis of Vascular Myocyte Time-Series and Line-Scan Ca Imaging Datasets.

Intracellular Ca signals are key for the regulation of cellular processes ranging from myocyte contraction, hormonal secretion, neural transmission, cellular metabolism, transcriptional regulation, and cell proliferation. Measurement of cellular Ca is routinely performed using fluorescence microscopy with biological indicators. Analysis of deterministic signals is reasonably straightforward as relevant data can be discriminated based on the timing of cellular responses.