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This Article Full Text Full Text (PDF) All Versions of this Article: 571/1/147    most recent jphysiol.2005.101394v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Snetkov, V. A. Articles by Aaronson, P. I. Search for Related Content PubMed PubMed Citation Articles by Snetkov, V. A. Articles by Aaronson, P. I. Related Collections Cardiovascular

¹ Department of Asthma, Allergy and Respiratory Science, King's College London School of Medicine, King's College London, London SE1 1UL, UK

The mechanisms by which prostaglandin F₂ (PGF₂) increases intracellular Ca²⁺ concentration [Ca²⁺]_i in vascular smooth muscle remain unclear. We examined the role of store-, receptor- and voltage-operated Ca²⁺ influx pathways in rat intrapulmonary arteries (IPA) loaded with Fura PE-3. Low concentrations (0.01–1 µM) of PGF₂ caused a transient followed by a plateau rise in [Ca²⁺]_i. Both responses became maximal at 0.1 µM PGF₂. At higher concentrations of PGF₂, a further slower rise in [Ca²⁺]_i was superimposed on the plateau. The [Ca²⁺]_i response to 0.1 µM PGF₂ was mimicked by the FP receptor agonist fluprostenol, whilst the effect of 10 µM PGF₂ was mimicked by the TP receptor agonist U-46619. The plateau rise in [Ca²⁺]_i in response to 0.1 µM PGF₂ was insensitive to diltiazem, and was abolished in Ca²⁺-free physiological salt solution, and by pretreatment with La³⁺, 2-APB, thapsigargin or U-73122. The rises in [Ca²⁺]_i in response to 10 µM PGF₂ and 0.01 µM U-46619 were partially inhibited by diltiazem. The diltiazem-resistant components of both of these responses were inhibited by 2-APB and La³⁺ to an extent which was significantly less than that seen for the response to 0.1 µM PGF₂, and were also much less sensitive to U-73122. The U-46619 response was also relatively insensitive to thapsigargin. When Ca²⁺ was replaced with Sr²⁺, the sustained increase in the Fura PE-3 signal to 0.1 µM PGF₂ was abolished, whereas 10 µM PGF₂ and 0.05 µM U-46619 still caused substantial increases. These results suggest that low concentrations of PGF₂ act via FP receptors to cause IP₃-dependent Ca²⁺ release and store operated Ca²⁺ entry (SOCE). U-46619 and 10–100 µM PGF₂ cause a TP receptor-mediated Ca²⁺ influx involving both L-type Ca²⁺ channels and a receptor operated pathway, which differs from SOCE in its susceptibility to La³⁺, 2-APB and thapsigargin, does not require phospholipase C activation, and is Sr²⁺ permeable.

(Received 7 November 2005; accepted after revision 12 December 2005; first published online 22 December 2005)
Corresponding author V. Snetkov: Department of Asthma, Allergy and Respiratory Science, New Hunt's House, Guy's Hospital Campus, King's College London, London SE1 1UL, UK. Email: vladimir.snetkov{at}kcl.ac.uk

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