A1-adenosine acute withdrawal response and cholecystokinin-8 induced contractures are regulated by Ca2+- and ATP-activated K+ channels

Maria Grazia Cascio, Daniela Valeri, Steven John Tucker, Pietro Marini (Corresponding Author)

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In isolated guinea-pig ileum (GPI), the A1-adenosine acute withdrawal response is under the control of several neuronal signalling systems, including the μ/κ-opioid and the cannabinoid CB1 systems. It is now well established that after the stimulation of the A1-adenosine system, the indirect activation of both μ/κ-opioid and CB1 systems is prevented by the peptide cholecystokinin-8 (CCk-8). In the present study, we have investigated the involvement of the Ca2+/ATP-activated K+ channels in the regulation of both acute A1-withdrawal and CCk-8-induced contractures in the GPI preparation. Interestingly, we found that: (a) the A1-withdrawal contracture is inhibited by voltage dependent Ca2+-activated K+ channels, Kv, while it is enhanced by the voltage independent Ca2+-activated K+ channels, SKCa; (b) in the presence of CCk-8, the inhibitory effect of the A1 agonist, CPA, on the peptide induced contracture is significantly enhanced by the voltage independent Ca2+-activated K+ channel, SKCa; and (c) the A1-withdrawal contracture precipitated in the presence of CCk-8 is controlled by the ATP-sensitive potassium channels, KATP. Our data suggest, for the first time, that both Ca2+- and ATP-activated K+ channels are involved in the regulation of both A1-withdrawal precipitated and CCk-8 induced contractures.
Original languageEnglish
Pages (from-to)82-91
Number of pages10
JournalPharmacological Research
Early online date30 Mar 2015
Publication statusPublished - May 2015



  • A1-adenosine receptor
  • A1-acute withdrawal
  • Cholecystokinin-8
  • Calcium-activated potassium channels
  • Adenosine triphosphate-activated potassium channels
  • Guinea-pig ileum

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