S-Space College of Medicine/School of Medicine (의과대학/대학원) Dept. of Physiology (생리학교실) Journal Papers (저널논문_생리학교실)
Bradykinin modulates pacemaker currents through bradykinin B2 receptors in cultured interstitial cells of Cajal from the murine small intestine
- Choi, Seok; Park, Do Young; Yeum, Cheol Ho; Chang, In Youb; You, Ho Jin; Park, Chan Guk; Kim, Man Yoo; Kong, In Deok; So, Insuk; Kim, Ki Whan; Jun, Jae Yeoul
- Issue Date
- Nature Publishing Group
- Br J Pharmacol. 2006 Aug;148(7):918-26. Epub 2006 Jun 19.
- Animals; Biological Clocks/*drug effects; Bradykinin/*pharmacology; Calcium/physiology; Calcium-Transporting ATPases/antagonists & inhibitors; Cells, Cultured; Chloride Channels/antagonists & inhibitors; Cyclooxygenase Inhibitors/pharmacology; Enzyme Inhibitors/pharmacology; Female; Intestine, Small/cytology/drug effects/*metabolism; Immunohistochemistry; Male; Mice; Mice, Inbred BALB C; Patch-Clamp Techniques; Protein Kinase C/antagonists & inhibitors; Receptor, Bradykinin B2/*drug effects; Signal Transduction/drug effects; Sodium/physiology
- We studied the modulation of pacemaker activities by bradykinin in cultured interstitial cells of Cajal (ICC) from murine small intestine with the whole-cell patch-clamp technique. Externally applied bradykinin produced membrane depolarization in the current-clamp mode and increased tonic inward pacemaker currents in the voltage-clamp mode. Pretreatment with bradykinin B1 antagonist did not block the bradykinin-induced effects on pacemaker currents. However, pretreatment with bradykinin B2 antagonist selectively blocked the bradykinin-induced effects. Also, only externally applied selective bradykinin B2 receptor agonist produced tonic inward pacemaker currents and ICC revealed a colocalization of the bradykinin B2 receptor and c-kit immunoreactivities, but bradykinin B1 receptors did not localize in ICC. External Na(+)-free solution abolished the generation of pacemaker currents and inhibited the bradykinin-induced tonic inward current. However, a Cl(-) channel blocker (DIDS) did not block the bradykinin-induced tonic inward current. The pretreatment with Ca(2+)-free solution and thapsigargin, a Ca(2+)-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker currents and suppressed the bradykinin-induced action.Chelerythrine and calphostin C, protein kinase C inhibitors or naproxen, an inhibitor of cyclooxygenase, did not block the bradykinin-induced effects on pacemaker currents. These results suggest that bradykinin modulates the pacemaker activities through bradykinin B2 receptor activation in ICC by external Ca(2+) influx and internal Ca(2+) release via protein kinase C- or cyclooxygenase-independent mechanism. Therefore, the ICC are targets for bradykinin and their interaction can affect intestinal motility.
- 0007-1188 (Print)
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