G-Protein regulation of an L-type calcium channel current in canine jejunal circular smooth muscle

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9 Citations (Scopus)

Abstract

Calcium entry into smooth muscle cells is essential to maintain contractility. In canine jejunal circular smooth muscle cells the predominant calcium entry pathway is through L-type calcium channels. The aim of this study was to determine the G-protein regulation of L-type calcium channel current (I(CaL)) in isolated canine jejunal circular smooth muscle cells. Barium (80 mM) was used as the charge carrier. GTP-γS and GTP increased maximal inward current from 118.7 ± 12 pA to 227.5 ± 21.5 pA (n = 8) and 174.6 ± 10.1 pA (n = 6) respectively. The increase in inward current was blocked bat nifedipine suggesting it was through L-type calcium channels. Pertussis toxin did not alter baseline I(CaL) while cholera toxin increased I(CaL) from 125 ± 19 pA in controls (n = 6) to 347 ± 30 pA (n = 4). Staurosporine inhibited the increase in current evoked by GTP-γS and calyculin further increased I,, over the increase evoked by GTP-γS. The results suggest that cholera toxin sensitive G-proteins activate L-type calcium channels in isolated canine jejunal circular smooth muscle cells through protein phosphorylation.

Original languageEnglish (US)
Pages (from-to)39-46
Number of pages8
JournalJournal of Membrane Biology
Volume160
Issue number1
DOIs
StatePublished - 1997

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L-Type Calcium Channels
Guanosine Triphosphate
GTP-Binding Proteins
Smooth Muscle Myocytes
Smooth Muscle
Canidae
Cholera Toxin
Calcium
Staurosporine
Pertussis Toxin
Barium
Nifedipine
Phosphorylation
Proteins

Keywords

  • Canine
  • G-proteins
  • Gastrointestinal smooth muscle
  • L-type calciun channels
  • Patch clamp

ASJC Scopus subject areas

  • Biophysics
  • Cell Biology
  • Physiology

Cite this

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title = "G-Protein regulation of an L-type calcium channel current in canine jejunal circular smooth muscle",
abstract = "Calcium entry into smooth muscle cells is essential to maintain contractility. In canine jejunal circular smooth muscle cells the predominant calcium entry pathway is through L-type calcium channels. The aim of this study was to determine the G-protein regulation of L-type calcium channel current (I(CaL)) in isolated canine jejunal circular smooth muscle cells. Barium (80 mM) was used as the charge carrier. GTP-γS and GTP increased maximal inward current from 118.7 ± 12 pA to 227.5 ± 21.5 pA (n = 8) and 174.6 ± 10.1 pA (n = 6) respectively. The increase in inward current was blocked bat nifedipine suggesting it was through L-type calcium channels. Pertussis toxin did not alter baseline I(CaL) while cholera toxin increased I(CaL) from 125 ± 19 pA in controls (n = 6) to 347 ± 30 pA (n = 4). Staurosporine inhibited the increase in current evoked by GTP-γS and calyculin further increased I,, over the increase evoked by GTP-γS. The results suggest that cholera toxin sensitive G-proteins activate L-type calcium channels in isolated canine jejunal circular smooth muscle cells through protein phosphorylation.",
keywords = "Canine, G-proteins, Gastrointestinal smooth muscle, L-type calciun channels, Patch clamp",
author = "Gianrico Farrugia",
year = "1997",
doi = "10.1007/s002329900293",
language = "English (US)",
volume = "160",
pages = "39--46",
journal = "Journal of Membrane Biology",
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T1 - G-Protein regulation of an L-type calcium channel current in canine jejunal circular smooth muscle

AU - Farrugia, Gianrico

PY - 1997

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N2 - Calcium entry into smooth muscle cells is essential to maintain contractility. In canine jejunal circular smooth muscle cells the predominant calcium entry pathway is through L-type calcium channels. The aim of this study was to determine the G-protein regulation of L-type calcium channel current (I(CaL)) in isolated canine jejunal circular smooth muscle cells. Barium (80 mM) was used as the charge carrier. GTP-γS and GTP increased maximal inward current from 118.7 ± 12 pA to 227.5 ± 21.5 pA (n = 8) and 174.6 ± 10.1 pA (n = 6) respectively. The increase in inward current was blocked bat nifedipine suggesting it was through L-type calcium channels. Pertussis toxin did not alter baseline I(CaL) while cholera toxin increased I(CaL) from 125 ± 19 pA in controls (n = 6) to 347 ± 30 pA (n = 4). Staurosporine inhibited the increase in current evoked by GTP-γS and calyculin further increased I,, over the increase evoked by GTP-γS. The results suggest that cholera toxin sensitive G-proteins activate L-type calcium channels in isolated canine jejunal circular smooth muscle cells through protein phosphorylation.

AB - Calcium entry into smooth muscle cells is essential to maintain contractility. In canine jejunal circular smooth muscle cells the predominant calcium entry pathway is through L-type calcium channels. The aim of this study was to determine the G-protein regulation of L-type calcium channel current (I(CaL)) in isolated canine jejunal circular smooth muscle cells. Barium (80 mM) was used as the charge carrier. GTP-γS and GTP increased maximal inward current from 118.7 ± 12 pA to 227.5 ± 21.5 pA (n = 8) and 174.6 ± 10.1 pA (n = 6) respectively. The increase in inward current was blocked bat nifedipine suggesting it was through L-type calcium channels. Pertussis toxin did not alter baseline I(CaL) while cholera toxin increased I(CaL) from 125 ± 19 pA in controls (n = 6) to 347 ± 30 pA (n = 4). Staurosporine inhibited the increase in current evoked by GTP-γS and calyculin further increased I,, over the increase evoked by GTP-γS. The results suggest that cholera toxin sensitive G-proteins activate L-type calcium channels in isolated canine jejunal circular smooth muscle cells through protein phosphorylation.

KW - Canine

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KW - Gastrointestinal smooth muscle

KW - L-type calciun channels

KW - Patch clamp

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