title: Endothelial [Ca2+]i is an integrating signal for the vascular tone in rat aortae.
abstract: BACKGROUND
  Although various endothelium-dependent relaxing factors (endothelial autacoids) are released upon the elevation of endothelial cytosolic free Ca2+ concentration (EC [Ca2+]i), the quantitative relationship between EC [Ca2+]i and vascular tone remains to be established. Moreover, whether the basal release of endothelial autacoids is modulated by basal EC [Ca2+]i is still unclear. We assessed these issues by using a novel method that allows simultaneous recording of EC [Ca2+]i and vascular displacement in dissected rat aortic segments.
  
  
  RESULTS
  Receptor-dependent (acetylcholine) or independent (ionomycin) agonists caused immediate EC [Ca2+]i elevation followed by vasorelaxation in preparations pre-contracted with phenylephrine. Low doses of agonists induced small EC [Ca2+]i elevations (about 100 nmol/L) and concomitant half-maximal vasorelaxation. At high doses, agonists elevated EC [Ca2+]i to micromol/L range with little additional vasodilatation. When EC [Ca2+]i was plotted against the vasorelaxation, the curves were almost identical for both acetylcholine and ionomycin treatments, in the presence or absence of various endothelial autacoid inhibitors. Calcium-free solution reduced basal EC [Ca2+]i and induced a drastic vasoconstriction. Endothelial autacoid inhibitors reduced EC [Ca2+]i changes and abolished both agonist-induced vasodilatation and calcium-free solution-induced vessel contraction. When the EC [Ca2+]i was completely chelated by 40 micromol/L BAPTA, the acetylcholine-evoked vasorelaxation could be abolished as well. However, when the EC [Ca2+]i was partially chelated by 20 micromol/L BAPTA, the acetylcholine-evoked vasorelaxation was almost unaffected.
  
  
  CONCLUSIONS
  These results indicate that vascular tone is modulated by subtle changes of EC [Ca2+]i level, which seems to serve as an integrating signal in both basal and stimulated states.
authors: Department of Physiology, National Cheng-Kung University Medical College, Tainan 701, Taiwan. s5887101@sparc1.cc.ncku.ed.tw
authors: T Y
authors: TY
authors: Huang
authors: H
authors: H
authors: Chen
authors: C Y
authors: CY
authors: Liu
authors: C J
authors: CJ
authors: Jen
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling; D046508:Culture Techniques; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D002118:Calcium