title: Tri-phasic modulation of ACh- and NA-maintained calcium plateau by high potassium in isolated mouse submandibular granular convoluted tubular cells.
abstract: OBJECTIVE
  The fact that submandibular glands secrete a large amount of potassium ion upon nerve stimulation has long been recognized, but a physiological role for such high potassium in the saliva has never been systematically investigated. In the present work, high potassium effect has been investigated in the freshly isolated mouse submandibular granular convoluted tubules.
  
  
  METHODS
  Isolated intact mouse submandibular granular convoluted tubules were loaded with Fura-2, and cytosolic calcium concentration in individual tubular cells was measured by microscopic fluorospectrometry.
  
  
  RESULTS
  It was found that high potassium had no effect on basal cytosolic calcium concentration, but had a tri-phasic modulation of the calcium plateau maintained by continued stimulation by acetylcholine (ACh) or noradrenaline (NA): a minor initial transient depression, followed by steady increase, completed by a robust calcium rebound spike upon removal of high potassium. The phase of steady increase was blocked without major effect on the plateau by KB-R 7943, a sodium/calcium exchange (NCX) inhibitor.
  
  
  CONCLUSIONS
  These data together suggest that high potassium in saliva bathing the mouse submandibular granular convoluted tubular cells has a potent feedback effect on ACh and NA stimulation, and sodium/calcium exchange is likely to play a major role in this process. Such positive feedback actions of high potassium may suggest a role for enhancing ACh- or NA-stimulated protein factor secretion from the granulated convoluted tubular cells.
authors.affiliation: Institute of Cell Biology, Beijing Normal University, Beijing 100875, China.
authors.forename: Yan Hong
authors.initials: YH
authors.lastname: Jia
authors.forename: Zong Jie
authors.initials: ZJ
authors.lastname: Cui
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D002614:Chelating Agents / Q000494:pharmacology; D025461:Feedback, Physiological; D016257:Fura-2 / Q000494:pharmacology; D008297:Male; D051379:Mice; D009638:Norepinephrine / Q000494:pharmacology / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000378:metabolism; D013363:Submandibular Gland / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism
chemical_list: D002614:Chelating Agents; D019831:Sodium-Calcium Exchanger; D012964:Sodium; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium; D016257:Fura-2; D009638:Norepinephrine