title: Endogenous testosterone increases leukocyte-endothelial cell interaction in spontaneously hypertensive rats.
abstract: OBJECTIVE
  Inflammation may have an important role in the beginning and in the progress of cardiovascular diseases. Testosterone exerts important effects on vascular function, which is altered in arterial hypertension. Thus, the aim of this study was to evaluate the influence of endogenous testosterone on leukocyte behavior in post-capillary venules of the mesenteric bed of spontaneously hypertensive rats (SHR).
  
  
  METHODS
  18 week-old intact SHR, castrated SHR and normotensive rats (intact Wistar) were used. Blood pressure was measured by tail plethysmography and serum testosterone levels by ELISA. Leukocyte rolling, adhesion and migration were evaluated in vivo in situ by intravital microscopy.
  
  
  RESULTS
  Castration significantly reduced blood pressure and reversed the increased leukocyte rolling and adhesion observed in SHRs. Leukocyte counts and other hemodynamic parameters did not differ among groups. SHRs displayed increased protein expression of P-selectin and ICAM-1 in mesenteric venules when compared to intact Wistar. Castration of SHRs restored the protein expression of the cell adhesion molecules.
  
  
  CONCLUSIONS
  The findings of the present study demonstrate the critical role of endogenous testosterone mediating the effects of hypertension increasing leukocyte-endothelial cell interaction. Increased expression of cell adhesion molecules contribute to the effects of endogenous testosterone promoting increased leukocyte rolling and adhesion in SHRs.
authors.affiliation: Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
authors.forename: F P
authors.initials: FP
authors.lastname: Filgueira
authors.forename: N S
authors.initials: NS
authors.lastname: Lobato
authors.forename: R A
authors.initials: RA
authors.lastname: DosSantos
authors.forename: M A
authors.initials: MA
authors.lastname: Oliveira
authors.forename: E H
authors.initials: EH
authors.lastname: Akamine
authors.forename: R C
authors.initials: RC
authors.lastname: Tostes
authors.forename: Z B
authors.initials: ZB
authors.lastname: Fortes
authors.forename: M H C
authors.initials: MH
authors.lastname: Carvalho
mesh_terms: D000818:Animals; D002448:Cell Adhesion; D002450:Cell Communication; D042783:Endothelial Cells / Q000166:cytology* / Q000276:immunology; D006439:Hemodynamics; D006973:Hypertension / Q000235:genetics / Q000276:immunology*; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000276:immunology; D036904:Leukocyte Rolling; D007962:Leukocytes / Q000166:cytology* / Q000276:immunology; D008297:Male; D009919:Orchiectomy; D019007:P-Selectin / Q000235:genetics / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D011918:Rats, Inbred SHR / Q000235:genetics / Q000276:immunology*; D017208:Rats, Wistar; D013739:Testosterone / Q000276:immunology*; D014699:Venules / Q000166:cytology
chemical_list: D019007:P-Selectin; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D013739:Testosterone