title: [Calcium induced calcium release from liver mitochondria of spontaneously hypertensive rats].
abstract: BACKGROUND
  Disturbances of ionic homeostasis of cells and recently discovered cellular energy deficiency due to reduced ATP-synthesizing ability of mitochondria are the most important components of pathogenesis of primary hypertension. Therefore it is essential to elucidate relationship between functioning of ionic transport systems especially that of calcium transport and ATP-synthesizing ability of mitochondria.
  
  
  OBJECTIVE
  To study calcium induced calcium release from liver mitochondria of spontaneously hypertensive rats at various initial calcium concentrations in medium.
  
  
  RESULTS
  We observed 30% lowering of maximal level of calcium uptake from the medium with unchanged rate of calcium uptake. Under conditions of calcium overload the rate of calcium release into the medium was 30% higher than in control.
  
  
  CONCLUSIONS
  These results evidenced for changes of functioning of mitochondrial permeability transition pores (MPT-pores) during calcium overload appearing as acceleration of their switch to high conductance mode and equilibration of all ionic gradients on internal mitochondrial membrane. This can negatively affect ATP-synthesizing ability of mitochondria. Thus the presence of linkage between disturbance of ionic homeostasis and intracellular energy deficit was confirmed.
authors.forename: E Iu
authors.initials: EIu
authors.lastname: Budnikov
authors.forename: A Iu
authors.initials: AIu
authors.lastname: Postnov
authors.forename: G V
authors.initials: GV
authors.lastname: Afanas'eva
authors.forename: A D
authors.initials: AD
authors.lastname: Doroshchuk
authors.forename: E V
authors.initials: EV
authors.lastname: Bus'ko
authors.forename: Iu V
authors.initials: IuV
authors.lastname: Postnov
mesh_terms: D000255:Adenosine Triphosphate / Q000096:biosynthesis*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D006706:Homeostasis; D006934:Hypercalcemia / Q000150:complications / Q000378:metabolism; D006973:Hypertension / Q000209:etiology / Q000378:metabolism*; D017136:Ion Transport; D008930:Mitochondria, Liver / Q000378:metabolism*; D051336:Mitochondrial Membranes / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013997:Time Factors
chemical_list: D000255:Adenosine Triphosphate; D002118:Calcium