Regulation of the cardiac L-type calcium channel in L6 cells by arginine-vasopressin

Basil M. Hantash, Andrew P. Thomas, John P. Reeves

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


L-type Ca2+ channel activity was measured in L6 cells as nifedipine-sensitive barium (Ba2+; 5 mM) influx in a depolarizing salt solution containing 140 mM KCl. Addition of AVP (arginine-vasopressin) during Ba2+ uptake reduced the rate of Ba2+ influx by 60-100%; this was followed by a gradual restoration of the initial rate of Ba2+ uptake. Blockade of PKC (protein kinase C) by pretreatment with 10 μM bisindolylmaleimide did not affect the initial inhibition of Ba 2+ influx, but completely abolished the recovery phase. The effect of AVP was half-maximal at 10 nM AVP and was blocked by the Via receptor antagonist d-(CH2)5-Tyr(Me)-AVP. Activation of G αs by isoprenaline or cholera toxin antagonized the actions of AVP on Ba2+ uptake. This protection persisted in the presence of the PKA (protein kinase A) inhibitor KT5720, and was not mimicked by agents that increase cAMP. Inhibition of Ba2+ influx was also elicited by ATP and ET (endothelin 1) with an order of effectiveness ET < ATP < AVP. Each of these agents has been reported to act through Gq-coupled receptors. We conclude that activation of Gq-coupled receptors produces a rapid inhibition of the cardiac L-type Ca2+ channel, which is subsequently overcome by activation of PKC.

Original languageEnglish (US)
Pages (from-to)411-419
Number of pages9
JournalBiochemical Journal
Issue number3
StatePublished - Dec 15 2006

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


  • Arginine-vasopressin (AVP)
  • Cardiac L-type calcium channel
  • G-protein
  • L6 cell
  • Protein kinase C (PKC)


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