title: Alkalization produced by high-dose carbachol in HSG cell line is independent of Ca2+.
abstract: OBJECTIVE
  The aim of this investigation was to clarify the mechanism of alkalization induced by carbachol in HSG cells.
  
  
  METHODS
  Cells of the HSG cell line derived from a human submandibular gland adenocarcinoma and those of the A-431 human epidermoid carcinoma cell line were loaded with a fluorescent pH indicator, BCECF/AM, and the change in the intracellular pH of adherent cells and suspended ones were measured following stimulation with various concentrations (10(-7) M to 10(-2) M) of neurotransmitters (carbachol, noradrenaline, and isoproterenol).
  
  
  RESULTS
  Isoproterenol did not cause alkalization of either cell type, whereas, noradrenaline and carbachol alkalized both types over the concentration ranges of 10(-6) M to 3 x 10(-3) M (HSG cell by noradrenaline), 10(-7) M to 2 x 10(-4) M (A-431 cell by noradrenaline), and 7 x 10(-5) M to 10(-4) M (A-431 cell by carbachol). On the other hand, alkalization induced by carbachol in the HSG cells was recognized at concentrations higher than 6 x 10(-5) M, and it showed no upper limit in terms of carbachol concentration. This high-dose carbachol alkalization was not eliminated by preincubation with nifedipine (100 microM), a Ca2+ channel blocker, or with thapsigargin (100 microM), a microsomal Ca(2+)-ATPase inhibitor.
  
  
  CONCLUSIONS
  The alkalization system induced by carbachol in the HSG cell was quite different from that in the A-431 cell, and that induced by high-dose carbachol in HSG cells appeared to be independent of intracellular Ca2+. These findings will be useful to clarify the mechanism of salivary secretion stimulated by neurotransmitters.
authors: Department of Oral Physiology, Meikai University, School of Dentistry, Saitama, Japan. tosi@dent.meikai.ac.jp
authors: T
authors: T
authors: Atsumi
authors: I
authors: I
authors: Iwakura
authors: T
authors: T
authors: Ueha
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects*; D000230:Adenocarcinoma / Q000378:metabolism; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D020013:Calcium Signaling; D002217:Carbachol / Q000494:pharmacology*; D002294:Carcinoma, Squamous Cell / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007545:Isoproterenol / Q000494:pharmacology; D018721:Muscarinic Agonists / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D012468:Salivary Gland Neoplasms / Q000378:metabolism*; D017923:Sodium-Hydrogen Exchangers / Q000819:agonists; D014407:Tumor Cells, Cultured / Q000187:drug effects
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D018721:Muscarinic Agonists; D017923:Sodium-Hydrogen Exchangers; D002217:Carbachol; D007545:Isoproterenol; D009638:Norepinephrine