title: Modulation of thiopental-induced vascular relaxation and contraction by perivascular adipose tissue and endothelium.
abstract: BACKGROUND
  Thiopental induces relaxation of vascular smooth muscle cells through its direct and/or indirect vasodilator effects. The perivascular adipose tissue (PVAT) and the endothelium are known to attenuate vascular contraction, and we have recently reported that PVAT potentiates the relaxation effect of propofol through endothelium-dependent and -independent mechanisms. Here, we studied the mechanisms of thiopental-induced vascular responses in relation to the involvement of PVAT and endothelium.
  
  
  METHODS
  Thoracic aortic rings from male Wistar rats were prepared with or without PVAT (PVAT+ and PVAT-) and with an intact endothelium (E+) or with the endothelium removed (E-) for functional studies. The contraction and relaxation responses of these vessels to thiopental in the presence of agonists and various receptor antagonists and channel blockers were studied.
  
  
  RESULTS
  In vessels pre-contracted with phenylephrine or KCl, thiopental-induced relaxation was highest in vessels denuded of both PVAT and the endothelium. PVAT attenuated the relaxation response to thiopental, and this attenuation effect was reduced by both angiotensin II (Ang II) type 1 receptor antagonists CV-11974 (2-n-butyl-4-choloro-5-hydroxymethyl-1-[2'-(1H-tetrazol-5-yl)biphenyl-methyl]-imidazole) or losartan and the angiotensin-converting enzyme inhibitor enalaprilat. Thiopental at high concentration (3 × 10(-3) M) caused a contraction through an endothelin-dependent mechanism.
  
  
  CONCLUSIONS
  Thiopental induced relaxation in rat aorta through an endothelium-independent pathway and the presence of PVAT, endothelium, or both attenuated this relaxation response through Ang II-dependent and endothelin-dependent mechanisms, respectively.
authors.affiliation: Department of Anesthesia,  McMaster University, Hamilton, Ontario,  Canada.
authors.forename: S I
authors.initials: SI
authors.lastname: Kassam
authors.forename: C
authors.initials: C
authors.lastname: Lu
authors.forename: N
authors.initials: N
authors.lastname: Buckley
authors.forename: Y J
authors.initials: YJ
authors.lastname: Gao
authors.forename: R M K W
authors.initials: RM
authors.lastname: Lee
mesh_terms: D000273:Adipose Tissue / Q000502:physiology*; D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D016232:Endothelins / Q000502:physiology; D004730:Endothelium, Vascular / Q000502:physiology*; D006162:Guanylate Cyclase / Q000502:physiology; D008297:Male; D010656:Phenylephrine / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013874:Thiopental / Q000494:pharmacology*; D046509:Tissue Culture Techniques; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D018686:Anesthetics, Intravenous; D016232:Endothelins; D015221:Potassium Channels; D014665:Vasodilator Agents; D000804:Angiotensin II; D010656:Phenylephrine; D011189:Potassium Chloride; D006162:Guanylate Cyclase; D013874:Thiopental