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Influence of Endogenous Testosterone on Vascular Endothelium‐Leukocyte Interaction in Spontaneously Hypertensive Rats (SHRs)
Author(s) -
Filgueira Fernando Paranaiba,
Lobato Núbia Souza,
Santos Rosângela Aparecida,
Oliveira Maria Aparecida,
Fortes Zuleica Bruno,
Tostes Rita,
Carvalho Maria Helena Catelli
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.934.5
Subject(s) - castration , medicine , endocrinology , endothelium , testosterone (patch) , endogeny , intravital microscopy , proinflammatory cytokine , inflammation , microcirculation , hormone
Aim Endogenous testosterone exerts influence on the vascular endothelium dysfunction in hypertension, and inflammation may play a important role in the onset and progress of cardiovascular diseases. So, we decided to evaluate the impact of castration on the leukocyte behavior in the SHR mesenteric post‐capillary venules. Methods and Results Male SHRs were castrated at 12 weeks of age and the leukocyte behavior was studied in vivo‐in situ by intravital microscopy. It was investigated after 6 weeks of orchidectomy and compared to the ones in the intact group. Castration reduced the number of leukocytes rolling and sticking along the venular endothelium, but not modified migrating after leukotriene B4 stimulation. P‐selectin protein expression (immunohistochemistry) as well as VCAM‐1 and PECAM‐1 gene expression (Real Time PCR) were reduced by castration and might be involved in the reduced rollers and stickers. However no difference was detected in ICAM‐1 protein and gene expression between groups. Venular shear rate, leukocyte and blood flow velocity, venular diameter and leukocyte counts were similar between groups. Castration reduced testosterone levels (EIA Kit) and blood pressure (tail pletismography). Conclusions Our results suggest that endogenous testosterone might has proinflammatory effect contributing to the development of vascular alterations in hypertension. FAPESP,CNPq/PRONEX,CAPES