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DOCA‐salt hypertension promotes leukocyte (but not platelet) adhesion in cerebral venules
Author(s) -
Rodrigues Stephen Fernandes,
Granger Daniel Neil
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.615.2
Subject(s) - platelet , medicine , ex vivo , pathogenesis , stroke (engine) , blood pressure , endocrinology , saline , venule , in vivo , p selectin , pathology , platelet activation , microcirculation , biology , mechanical engineering , microbiology and biotechnology , engineering
Although hypertension is a major risk factor for the development of ischemic stroke, the mechanisms underlying the influence of increased blood pressure on stroke risk remain poorly understood. Since both platelets and inflammatory cells have been implicated in the pathogenesis of ischemic stroke, we examined whether DOCA‐salt induced hypertension alters the behavior of platelets and leukocytes in cerebral venules in male mice. A 50 mg DOCA pellet was implanted via s.c. in uninephrectomized C57Bl/6 mice placed on 1 % saline for a period of 3 weeks, which produced a significant increase in blood pressure (from 103±2 to 127±2 mmHg) as well as cardiac and renal hypertrophy (relative to controls). Platelets isolated from matched donor mice were labeled ex vivo with CSFE while rhodamine was administered i.v. for in vivo labeling of leukocytes. Intravital microscopic observation of blood cell trafficking in pial venules revealed a large increase in the number of adherent leukocytes in DOCA‐salt mice (558±58 per mm 2 vs 183±39 per mm 2 ). However, platelet adhesion within venules was unaffected by DOCA‐salt (12±7 per mm 2 vs 4±4 per mm 2 ). These findings indicate that DOCA‐salt induced hypertension induced a pro‐inflammatory, but not a pro‐thrombogenic, phenotype in the cerebral microvasculature. The accumulation of inflammatory cells in the brain during hypertension may predispose this tissue to ischemic tissue injury. (Supported by HL26441).