Impairment of selectin-mediated leukocyte adhesion to venular endothelium in spontaneously hypertensive rats.

@article{Suematsu1995ImpairmentOS,
  title={Impairment of selectin-mediated leukocyte adhesion to venular endothelium in spontaneously hypertensive rats.},
  author={Makoto Suematsu and H. Suzuki and Takuya Tamatani and Yutaka Iigou and Frank A. Delano and Masayuki Miyasaka and Michael J. Forrest and Reiji Kannagi and Benjamin W. Zweifach and Yuzuru Ishimura},
  journal={The Journal of clinical investigation},
  year={1995},
  volume={96 4},
  pages={
          2009-16
        }
}
The present study was designed to elucidate whether molecular mechanisms for leukocyte adhesion to microvascular endothelium may differ between spontaneously hypertensive rats and Wistar Kyoto rats. Leukocyte rolling and adhesion were investigated while monitoring venular wall shear rates in the mesenteric microcirculation stimulated with histamine or tert-butyl hydroperoxide in the two strains. In Wistar Kyoto rats, 10 microM histamine as well as 500 microM tertbutyl hydroperoxide promoted a… 
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Background Citations
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Methods Citations
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Results Citations
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48 Citations

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Citation Type

Role of CD18-ICAM-1 in the entrapment of stimulated leukocytes in alveolar capillaries of perfused rat lungs.
TLDR
The results suggest that selectin-independent, CD18-ICAM-1-dependent capillary sequestration is one of the major mechanisms by which activated leukocytes accumulate in the lungs.
Hydralazine reduces leukocyte migration through different mechanisms in spontaneously hypertensive and normotensive rats.
Receptor cleavage and P‐selectin‐dependent reduction of leukocyte adhesion in the spontaneously hypertensive rat
TLDR
The attenuated rolling interactions of SHR leukocytes with the endothelium were restored by chronic treatment with a broad‐spectrum MMP inhibitor (CGS) for 24 weeks, and the SHR MMP levels decreased significantly with treatment.
Constitutive Expression and Enzymatic Cleavage of ICAM-1 in the Spontaneously Hypertensive Rat
TLDR
Intercellular adhesion molecule expression in SHRs is upregulated in a tissue-specific manner, which suggests that enzymatic cleavage may be a factor determining ICAM-1 distribution and may play a role in the renal involvement of inflammation.
Constitutive Expression and Enzymatic Cleavage of ICAM-1 in the Spontaneously Hypertensive Rat
TLDR
The liver and kidney glomeruli exhibit a discrepancy in label density between intra- and extracellular antibodies, which suggests that enzymatic cleavage may be a factor determining ICAM-1 distribution.
Immunoneutralization of glycoprotein Ibalpha attenuates endotoxin-induced interactions of platelets and leukocytes with rat venular endothelium in vivo.
TLDR
These results provide the first evidence for involvement of GP Ibalpha in endotoxin-induced microvascular rolling of platelets and leukocytes, and this system serves as a potentially useful tool to examine GP I Balpha-associated function of human platelets in vivo.
Leukocyte-Endothelium Interaction in the Rat Mesenteric Microcirculation during Halothane or Sevoflurane Anesthesia
TLDR
Halothane or sevoflurane anesthesia induces venular leukocyte rolling and adhesion, whereas low-flow perfusion is likely to evoke ICAM-1-dependent leukocytes adhesion during halothane anesthesia.
Induction of heme oxygenase-1 suppresses venular leukocyte adhesion elicited by oxidative stress: role of bilirubin generated by the enzyme.
TLDR
Results indicate that induction of the HO-1 activity serves as a potential stratagem to prevent oxidant-induced microvascular leukocyte adhesion through the action of bilirubin, a product of HO reaction.
Experimental studies on the role of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1 in hypertensive nephrosclerosis.
TLDR
The data suggest that ICAM-1 is involved in the recruitment of macrophages/lymphocytes via specific interaction of IC AM-1 and LFA-1 in this model of hypertensive target-organ damage.
ETA Receptor Mediates Altered Leukocyte-Endothelial Cell Interaction and Adhesion Molecules Expression in DOCA–Salt Rats
TLDR
Data indicate that ET-1 participates, via activation of ETA receptors, in altered leukocyte–endothelial cell interactions in DOCA–salt rats, possibly by modulating expression of CAMs, and that the inflammatory status is associated with cardiac damage in mineralocorticoid hypertension.
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References

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