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

作者：Cascio Maria Grazia; Valeri Daniela; Tucker Steven J; Marini Pietro^*

来源：Pharmacological Research, 2015, 95-96: 82-91.

DOI：10.1016/j.phrs.2015.03.014

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

In isolated guinea-pig ileum (GPI), the A1-adenosine acute withdrawal response is under the control of several neuronal signalling systems, including the mu/kappa-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 mu/kappa-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, K-V, 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, K-ATP. 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.

• 出版日期2015-6
• 单位河北医科大学