P2-purinergic stimulation of iodide efflux in FRTL-5 rat thyroid cells involves parallel activation of PLC and PLA2

R. C. Smallridge, I. D. Gist

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Extracellular ATP increases inositol phosphates, cytosolic Ca2+ concentration ([Ca2+](i)), arachidonic acid (AA) release, and iodide efflux in FRTL-5 cells. To examine the sequence of events in P2-purinergic receptor activation by ATP, a phospholipase C (PLC) inhibitor (U-73122), and a phospholipase A2 (PLA2) inhibitor (U-26384), as well as 1,2-bis(2- aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) and downregulation of protein kinase C (PKC) were used. ATP increased inositol trisphosphate (IP3), [Ca2+](i), AA release, and 125I efflux dose dependently. U- 73122 inhibited the IP3 and calcium increase but not AA; U-26384 prevented AA release but not the increase in calcium. Both agents inhibited iodide efflux. BAPTA prevented any ATP-induced increase in [Ca2+](i) without affecting AA release or 125I efflux. PKC downregulation had no effect on ATP stimulated AA release, but reduced 125I efflux: We conclude that ATP- induced iodide efflux involves parallel, not sequential, activation of PLC and PLA2. No increase in [Ca2+](i) or PKC activity is required for PLA2 activation. In contrast, an increase in 125I efflux depends on PKC and PLA2 activities, but not an increase in [Ca2+](i).

Original languageEnglish (US)
Pages (from-to)E323-E330
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number2 30-2
StatePublished - 1994
Externally publishedYes


  • adenosine 5'-triphosphate
  • arachidonic acid
  • cytosolic calcium
  • inositol trisphosphate
  • phospholipase A
  • phospholipase C
  • protein kinase C
  • thyroid

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)


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