title: Decreased vascular reactivity to alpha1 adrenergic stimulation in the presence of hypothyroid state: a part of an adaptive response?
abstract: OBJECTIVE
  A hypothyroid state frequently accompanies cardiac illnesses but its physiological significance for the cardiovascular hemodynamics remains largely unknown. Therefore, the present study investigated possible physiological consequences on vascular function in an experimental model of low thyroid hormone state.
  
  
  METHODS
  Hypothyroidism was induced in rats by the administration of 6-n-propyl-2-thiouracil in drinking water (final concentration of 0.05%) for 3 weeks, HYPO rats, and untreated rats served as controls (Control). Isolated aortic rings with or without endothelium (E+, E-) were contracted with KCl (10 to 60 mM) and phenylephrine (PE) (10(-10) to 10(-5) M). Maximal tension (Tmax) in g and EC(50) in response to PE and KCl were measured.
  
  
  RESULTS
  Tmax was significantly lower while EC(50) was significantly higher in response to PE in HYPO(E+) than in Control(E+). Upon endothelium removal, Tmax was not significantly different between the groups but EC(50) was still significantly higher in HYPO(E-) than in Control(E-). EC(50) in response to KCl was significantly higher in HYPO with or without endothelium and no difference was found in Tmax.
  
  
  CONCLUSIONS
  Hypothyroid aortic rings respond less to a1 adrenergic stimulation probably due to the endothelium modulatory effect as well as to intrinsic smooth muscle defect. This seems to be of important clinical relevance.
authors.affiliation: Department of Pharmacology, University of Athens, Athens, Greece. cpantos@cc.uoa.gr
authors.forename: C
authors.initials: C
authors.lastname: Pantos
authors.forename: C
authors.initials: C
authors.lastname: Mourouzis
authors.forename: M
authors.initials: M
authors.lastname: Katramadou
authors.forename: T
authors.initials: T
authors.lastname: Saranteas
authors.forename: I
authors.initials: I
authors.lastname: Mourouzis
authors.forename: H
authors.initials: H
authors.lastname: Karageorgiou
authors.forename: C
authors.initials: C
authors.lastname: Tesseromatis
authors.forename: G
authors.initials: G
authors.lastname: Kostopanagiotou
authors.forename: P
authors.initials: P
authors.lastname: Asimacopoulos
authors.forename: D V
authors.initials: DV
authors.lastname: Cokkinos
mesh_terms: D000220:Adaptation, Biological / Q000502:physiology*; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000503:physiopathology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D007037:Hypothyroidism / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D010656:Phenylephrine / Q000494:pharmacology*; D011189:Potassium Chloride / Q000494:pharmacology*; D051381:Rats; D018340:Receptors, Adrenergic, alpha-1 / Q000187:drug effects* / Q000378:metabolism; D013963:Thyroid Hormones / Q000097:blood; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D000316:Adrenergic alpha-Agonists; D018340:Receptors, Adrenergic, alpha-1; D013963:Thyroid Hormones; D010656:Phenylephrine; D011189:Potassium Chloride