Sphingosylphosphorylcholine-induced vasoconstriction of pulmonary artery: Activation of non-store-operated Ca(2+) entry

G  D Thomas; V  A Snetkov; R Patel; R  M Leach; P  I Aaronson; J  P Ward

doi:10.1016/j.cardiores.2005.05.013

Sphingosylphosphorylcholine-induced vasoconstriction of pulmonary artery: Activation of non-store-operated Ca(2+) entry

G D Thomas, V A Snetkov, R Patel, R M Leach, P I Aaronson, J P Ward

King's College London

Research output: Contribution to journal › Article › peer-review

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Abstract

OBJECTIVE: Sphingosylphosphorylcholine (SPC) is an important lipid mediator that has been implicated in vascular disease. As it has not been studied in the pulmonary circulation, we examined its mechanisms of action in rat small intrapulmonary arteries (IPA). METHODS: IPA were mounted on a myograph for recording tension and intracellular Ca(2+) concentration ([Ca(2+)](i)). Ca(2+) sensitisation was examined in alpha-toxin permeabilized IPA, and by Western blot analysis of MYPT1 phosphorylation. RESULTS: SPC induced a slow but powerful vasoconstriction in IPA associated with an elevation in [Ca(2+)](i), with an EC(50) for vasoconstriction of 12+/-2 muM. Removal of extracellular Ca(2+) increased the EC(50) to 76+/-33 muM (p

Original language	English
Pages (from-to)	56 - 64
Number of pages	9
Journal	Cardiovascular Research
Volume	68
Issue number	1
DOIs	https://doi.org/10.1016/j.cardiores.2005.05.013
Publication status	Published - 1 Oct 2005

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title = "Sphingosylphosphorylcholine-induced vasoconstriction of pulmonary artery: Activation of non-store-operated Ca(2+) entry",

abstract = "OBJECTIVE: Sphingosylphosphorylcholine (SPC) is an important lipid mediator that has been implicated in vascular disease. As it has not been studied in the pulmonary circulation, we examined its mechanisms of action in rat small intrapulmonary arteries (IPA). METHODS: IPA were mounted on a myograph for recording tension and intracellular Ca(2+) concentration ([Ca(2+)](i)). Ca(2+) sensitisation was examined in alpha-toxin permeabilized IPA, and by Western blot analysis of MYPT1 phosphorylation. RESULTS: SPC induced a slow but powerful vasoconstriction in IPA associated with an elevation in [Ca(2+)](i), with an EC(50) for vasoconstriction of 12+/-2 muM. Removal of extracellular Ca(2+) increased the EC(50) to 76+/-33 muM (p",

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T1 - Sphingosylphosphorylcholine-induced vasoconstriction of pulmonary artery: Activation of non-store-operated Ca(2+) entry

AU - Thomas, G D

AU - Snetkov, V A

AU - Patel, R

AU - Leach, R M

AU - Aaronson, P I

AU - Ward, J P

PY - 2005/10/1

Y1 - 2005/10/1

N2 - OBJECTIVE: Sphingosylphosphorylcholine (SPC) is an important lipid mediator that has been implicated in vascular disease. As it has not been studied in the pulmonary circulation, we examined its mechanisms of action in rat small intrapulmonary arteries (IPA). METHODS: IPA were mounted on a myograph for recording tension and intracellular Ca(2+) concentration ([Ca(2+)](i)). Ca(2+) sensitisation was examined in alpha-toxin permeabilized IPA, and by Western blot analysis of MYPT1 phosphorylation. RESULTS: SPC induced a slow but powerful vasoconstriction in IPA associated with an elevation in [Ca(2+)](i), with an EC(50) for vasoconstriction of 12+/-2 muM. Removal of extracellular Ca(2+) increased the EC(50) to 76+/-33 muM (p

AB - OBJECTIVE: Sphingosylphosphorylcholine (SPC) is an important lipid mediator that has been implicated in vascular disease. As it has not been studied in the pulmonary circulation, we examined its mechanisms of action in rat small intrapulmonary arteries (IPA). METHODS: IPA were mounted on a myograph for recording tension and intracellular Ca(2+) concentration ([Ca(2+)](i)). Ca(2+) sensitisation was examined in alpha-toxin permeabilized IPA, and by Western blot analysis of MYPT1 phosphorylation. RESULTS: SPC induced a slow but powerful vasoconstriction in IPA associated with an elevation in [Ca(2+)](i), with an EC(50) for vasoconstriction of 12+/-2 muM. Removal of extracellular Ca(2+) increased the EC(50) to 76+/-33 muM (p

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DO - 10.1016/j.cardiores.2005.05.013

M3 - Article

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JO - Cardiovascular Research

JF - Cardiovascular Research

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Sphingosylphosphorylcholine-induced vasoconstriction of pulmonary artery: Activation of non-store-operated Ca(2+) entry

Abstract

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