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This Article Full Text Full Text (PDF) All Versions of this Article: 293/5/L1135    most recent 00432.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Paffett, M. L. Articles by Walker, B. R. Search for Related Content PubMed PubMed Citation Articles by Paffett, M. L. Articles by Walker, B. R.

Reduced store-operated Ca²⁺ entry in pulmonary endothelial cells from chronically hypoxic rats

Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico

Submitted 1 November 2006 ; accepted in final form 6 August 2007

Chronic hypoxia (CH)-induced pulmonary hypertension may influence basal endothelial cell (EC) intracellular Ca²⁺ concentration ([Ca²⁺]_i). We hypothesized that CH decreases EC [Ca²⁺]_i associated with membrane depolarization and reduced Ca²⁺ entry. To test this hypothesis, we assessed 1) basal endothelial Ca²⁺ in pressurized pulmonary arteries and freshly isolated ECs, 2) EC membrane potential (E_m), 3) store-operated Ca²⁺ current (I_SOC), and 4) store-operated Ca²⁺ (SOC) entry in arteries from control and CH rats. We found that basal EC Ca²⁺ was significantly lower in pressurized pulmonary arteries and freshly isolated ECs from CH rats compared with controls. Similarly, ECs in intact arteries from CH rats were depolarized compared with controls, although no differences were observed between groups in isolated cells. I_SOC activation by 1 µM thapsigargin displayed diminished inward current and a reversal potential closer to 0 mV in cells from CH rats compared with controls. In addition, SOC entry determined by fura 2 fluorescence and Mn²⁺ quenching revealed a parallel reduction in Ca²⁺ entry following CH. We conclude that differences in the magnitude of SOC entry exist between freshly dispersed ECs from CH and control rats and correlates with the decrease in basal EC [Ca²⁺]_i. In contrast, basal EC Ca²⁺ influx is unaffected and membrane depolarization is limited to intact arteries, suggesting that E_m may not play a major role in determining basal EC [Ca²⁺]_i following CH.

pulmonary hypertension; electrochemical gradient and calcium entry