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Sodium–Calcium Exchanger in Pulmonary Artery Smooth Muscle Cells
Author(s) -
ZHENG YUNMIN,
WANG YONGXIAO
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1387.017
Subject(s) - sodium calcium exchanger , intracellular , pulmonary artery , depolarization , myocyte , calcium in biology , medicine , endoplasmic reticulum , homeostasis , chemistry , patch clamp , endocrinology , microbiology and biotechnology , biology , electrophysiology
The expression and function of the Na + /Ca 2+ exchanger (NCX) in the regulation of intracellular Ca 2+ homeostasis have been well studied in cardiac, skeletal, and systemic vascular myocytes, but not in pulmonary artery smooth muscle cells (SMCs). We have recently demonstrated that the NCX current is present in freshly isolated pulmonary artery SMCs using the patch‐clamp technique. The current has a mean amplitude of 13 pA under near physiological resting conditions. The NCX may function in the forward mode to make a significant contribution to the decay of intracellular Ca 2+ following Ca 2+ release and/or depolarization. Hypoxic stimulation inhibits the NCX current, reduces the removal of intracellular Ca 2+ , and enhances Ca 2+ release from the sarcoplsamic reticulum. Using RT‐PCR, subcloning and sequence analysis, we have shown that three NCX1 splice variants: NCX1.2 (containing exons B, C, and D), NCX1.3 (exons B and D), and NCX1.7 (exons B, D, and F) are expressed in pulmonary artery smooth muscle. Each of these splice variants expressed in HEK293 cells it likely to show a distinct activity in the removal of intracellular Ca 2+ . Taken together, we provide clear evidence that NCX1 is functionally and molecularly expressed and plays a physiological role in pulmonary artery SMCs.