title: Tributyltin impairs the coronary vasodilation induced by 17β-estradiol in isolated rat heart.
abstract: Triorganotins, such as tributyltin (TBT), are environmental contaminants that are commonly used as antifouling agents for boats. However, TBT is also known to alter mammalian reproductive functions. Although the female sex hormones are primarily involved in the regulation of reproductive functions, 17β-estradiol also protects against cardiovascular diseases, in that this hormone reduces the incidence of coronary artery disease via coronary vasodilation. The aim of this study was to examine the influence of 100 ng/kg TBT administered daily by oral gavage for 15 d on coronary functions in female Wistar rats. Findings were correlated with changes in sex steroids concentrations. Tributyltin significantly increased the baseline coronary perfusion pressure and impaired vasodilation induced by 17β-estradiol. In addition, TBT markedly decreased serum 17β-estradiol levels accompanied by a significant rise in serum progesterone levels. Tributyltin elevated collagen deposition in the heart interstitium and number of mast cells proximate to the cardiac vessels. There was a positive correlation between the increase in coronary perfusion pressure and incidence of cardiac hypertrophy. In addition, TBT induced endothelium denudation (scanning electron microscopy) and accumulation of platelets. Moreover, TBT impaired coronary vascular reactivity to estradiol (at least in part), resulting in endothelial denudation, enhanced collagen deposition and elevated number of mast cells. Taken together, the present results demonstrate that TBT exposure may be a potential risk factor for cardiovascular disorders in rats.
authors.affiliation: Department of Physiology, Federal University of Espirito Santo-UFES, Espírito Santo, Brazil.
authors.forename: Roger Lyrio
authors.initials: RL
authors.lastname: dos Santos
authors.forename: Priscila Lang
authors.initials: PL
authors.lastname: Podratz
authors.forename: Gabriela Cavati
authors.initials: GC
authors.lastname: Sena
authors.forename: Vicente Sathler Delgado
authors.initials: VS
authors.lastname: Filho
authors.forename: Pedro Francisco Iguatemy
authors.initials: PF
authors.lastname: Lopes
authors.forename: Washington Luiz Silva
authors.initials: WL
authors.lastname: Gonçalves
authors.forename: Leandro Miranda
authors.initials: LM
authors.lastname: Alves
authors.forename: Vivian Yochiko
authors.initials: VY
authors.lastname: Samoto
authors.forename: Christina Maeda
authors.initials: CM
authors.lastname: Takiya
authors.forename: Emilio
authors.initials: E
authors.lastname: de Castro Miguel
authors.forename: Margareth Ribeiro
authors.initials: MR
authors.lastname: Moysés
authors.forename: Jones Bernardes
authors.initials: JB
authors.lastname: Graceli
mesh_terms: D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004347:Drug Interactions; D004730:Endothelium, Vascular / Q000187:drug effects / Q000648:ultrastructure; D004785:Environmental Pollutants / Q000633:toxicity*; D004958:Estradiol / Q000008:administration & dosage / Q000493:pharmacokinetics*; D005260:Female; D051381:Rats; D017208:Rats, Wistar; D014220:Trialkyltin Compounds / Q000633:toxicity*; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D004785:Environmental Pollutants; D014220:Trialkyltin Compounds; D004958:Estradiol; C011559:tributyltin