Hypertension is associated with a progressive organ injury whose etiol
ogy remains largely speculative. An increasing database shows that act
ivated leukocytes, while affording an important immune protection, may
be a contributing factor to several of the pathogenetic features of t
he hypertension syndrome. The purpose of this study was to determine t
he extent to which the glucocorticoid pathway may be involved in the a
typical kinetics of leukocytes in spontaneously hypertensive rats (SHR
) compared with normotensive Wistar-Kyoto (WKY) rats. The typical venu
lar leukocyte adhesion induced by histamine application was significan
tly lower in SHR, and a comparison of normalized leukocyte rolling vel
ocity (V-WBC/V-RBC) showed the values to be significantly higher in SH
R relative to WKY controls. This abnormal trend in adherent leukocyte
numbers and in V-WBC/V-RBC values could be counteracted when SHR were
pretreated with RU 486, a synthetic glucocorticoid inhibitor, and rest
ored to the levels observed in WKY rats. Anti-P-selectin monoclonal an
tibody (PB1.3) attenuated in SHR and WKY rats the increment of adheren
t leukocyte numbers as well as the decrement of V-WBC/ V-RBC value tha
t developed under combined histamine and RU 486 superfusion. Furthermo
re, an anti-intercellular adhesion molecule-1 monoclonal antibody (1A2
9) served to attenuate the increment of adherent leukocyte number indu
ced by a combination of histamine and RU 486 superfusion in WKY rats a
nd SHR. The results indicate that the deficient leukocyte-endothelial
cell interaction in SHR can be circumvented by a glucocorticoid inhibi
tor.