title: Ca2+ mobilization by vasopressin and glucagon in perfused livers. Effect of prior intoxication with bromotrichloromethane.
abstract: Perfused livers isolated from rats treated with BrCCl3 for up to 15 min were used as an experimental tool to investigate the role of the hepatic endoplasmic reticulum in Ca2+ mobilization elicited by vasopressin and glucagon. BrCCl3-treatment caused extensive impairment (37 to 92%) of Ca2+ pumps of isolated liver microsomes, while Ca2+ pumps of mitochondria and plasma membrane vesicles remained undamaged. In perfused livers of BrCCl3-treated rats, the efflux of Ca2+ and the concomitant stimulation of O2 consumption and glucose release induced by vasopressin were decreased. The extent of the decrease paralleled the duration of BrCCl3-treatment. The decrease of Ca2+ efflux following vasopressin addition was closely correlated with the decrease of active Ca2+ accumulation by isolated microsomes (r = 0.99, P less than 0.001). The Ca2+ efflux elicited by glucagon was also decreased after BrCCl3-treatment, whereas stimulation of O2 consumption and glucose release were retained. The possibility that BrCCl3-treatment might impair the production of the intracellular Ca2+-mobilizing messenger IP3 is unlikely, since vasopressin still induced the formation of inositol phosphates, including IP3, in isolated hepatocytes obtained from BrCCl3-treated rats. Thus, this work supports the hypothesis that the Ca2+ stored in the liver ER is the major pool of intracellular Ca2+ available for mobilization by vasopressin, glucagon and other effectors.
authors.affiliation: Institute of General Pathology, University of Siena, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Benedetti
authors.forename: P
authors.initials: P
authors.lastname: Graf
authors.forename: R
authors.initials: R
authors.lastname: Fulceri
authors.forename: A
authors.initials: A
authors.lastname: Romani
authors.forename: H
authors.initials: H
authors.lastname: Sies
mesh_terms: D000818:Animals; D001975:Bromotrichloromethane / Q000633:toxicity*; D002118:Calcium / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism; D002725:Chloroform / Q000031:analogs & derivatives*; D005934:Glucagon / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D007295:Inositol Phosphates / Q000378:metabolism; D008099:Liver / Q000187:drug effects*; D008862:Microsomes, Liver / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D014667:Vasopressins / Q000494:pharmacology*
chemical_list: D007295:Inositol Phosphates; D014667:Vasopressins; D002725:Chloroform; D005934:Glucagon; D001975:Bromotrichloromethane; D005947:Glucose; D002118:Calcium