title: Phenylephrine induced aortic vasoconstriction is attenuated in hyperthyroid rats.
abstract: BACKGROUND
  Abnormal vascular responsiveness to vasoconstrictors may play an important role in peripheral vascular resistance in hyperthyroidism. The aim of the present study was to evaluate whether the vascular response to potassium chloride and phenylephrine is abnormal in a rat model of thyroxine-induced cardiac hypertrophy.
  
  
  METHODS
  Left ventricular hypertrophy was induced in Wistar rats by subcutaneous administration of L-thyroxine for two weeks ("THYR"), n=17. Animals treated with normal saline served as controls, ("NORM"), n=20. The thoracic aorta was dissected and cut into rings that were suspended in an isolated organ bath with Krebs-Henseleit buffer. Maximal tension, Tmax, in g was measured in response to KCl and PE at the highest concentration in rings with endothelium (+E) and without endothelium (-E) in both groups. Relaxation response (Relax percent) to acetylcholine administration was expressed as percent of the maximal tension induced by phenylephrine.
  
  
  RESULTS
  Left ventricular weight was 0.9 (SEM, 0.04) g for THYR group vs 0.7 (0.02) g for the NORM group, p<0.05. With KCl, Tmax was not different between the THYR and NORM groups with and without endothelium. With PE, there was a difference in Tmax between THYR+E and NORM+E, 1.2 (0.05) g vs 1.5 (0.09) g, p<0.05. Tmax was also different between THYR-E and NORM-E, 1.5 (0.08) g vs 1.7 (0.07) g, p<0.05. Relax percent was not significantly different between THYR+E and NORM+E (45.9 percent vs 42.8 percent, p>0.05).
  
  
  CONCLUSIONS
  We conclude that: a) Vascular tension of the thoracic aorta in response to PE is lower in thyroxine-treated rats as compared to controls, probably due to enhanced PE-induced vasorelaxation at high concentration. b) Relaxation response of the thoracic aorta to acetylcholine is not different between THYR and NORM groups.
authors.affiliation: Department of Pharmacology, University of Athens, Athens, Greece.
authors.forename: C I
authors.initials: CI
authors.lastname: Pantos
authors.forename: V
authors.initials: V
authors.lastname: Tzilalis
authors.forename: S
authors.initials: S
authors.lastname: Giannakakis
authors.forename: D D
authors.initials: DD
authors.lastname: Cokkinos
authors.forename: S M
authors.initials: SM
authors.lastname: Tzeis
authors.forename: V
authors.initials: V
authors.lastname: Malliopoulou
authors.forename: I
authors.initials: I
authors.lastname: Mourouzis
authors.forename: P
authors.initials: P
authors.lastname: Asimakopoulos
authors.forename: H
authors.initials: H
authors.lastname: Carageorgiou
authors.forename: D D
authors.initials: DD
authors.lastname: Varonos
authors.forename: D V
authors.initials: DV
authors.lastname: Cokkinos
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects*; D006332:Cardiomegaly / Q000097:blood / Q000150:complications; D004730:Endothelium, Vascular / Q000187:drug effects; D006980:Hyperthyroidism / Q000097:blood* / Q000150:complications; D008297:Male; D023421:Models, Animal; D009131:Muscle, Smooth, Vascular / Q000098:blood supply*; D009200:Myocardial Contraction / Q000187:drug effects; D010656:Phenylephrine / Q000494:pharmacology*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013974:Thyroxine / Q000008:administration & dosage; D014661:Vasoconstriction / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D010656:Phenylephrine; D011189:Potassium Chloride; D000109:Acetylcholine; D013974:Thyroxine