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Entanercept reduces vessel remodeling in stroke prone spontaneously hypertensive rats
Author(s) -
Dorrance Anne M,
Poulsen Kyle L,
McClain Jonathon L,
Pires Paulo W
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.805.11
Subject(s) - medicine , blood pressure , lumen (anatomy) , proinflammatory cytokine , inflammation , blood vessel , endocrinology , cardiology
Inflammation plays a key role in the pathogenesis of hypertension. Hypertension results in resistance vessel remodeling which includes an increased vessel wall thickness and wall / lumen ratio. We hypothesized that inhibition of the proinflammatory cytokine, tumor necrosis factor‐α (TNF‐α) with the etanercept (ETN) would prevent vessel remodeling in stroke prone spontaneously hypertensive rats (SHRSP). Six‐week‐old SHRSP were treated with ETN (1.25mg/kg/day I.P.) for six weeks, after which blood pressure was measured and third order mesenteric arteries were removed for assessment of vessel structure by pressure myography. The results are presented as mean ± SEM. There was no difference in the body weight (253.4±6.6 vs 246.3±4.8 grams, control vs ETN) or blood pressure (206±9 vs 198±3mmHg, control vs ETN) between the control and ETN treated rats. At an intralumenal pressure of 60mmHg, ETN treatment significantly reduced the vessel wall thickness (31.9±1.8 vs 26.5±1.3μm control vs ETN p<0.05) and wall / lumen ratio (0.13±0.01 vs 0.10±0.003 control vs ETN p<0.05). Vessel wall stiffness was also reduced in the ETN treated rats as evidenced by a reduction in the β coefficient calculated from the individual stress / strain curves (5.45±0.39 vs 4.58±0.20 control vs ETN p<0.05). These results suggest that TNF‐α mediated inflammation contributes to the vessel remodeling process in a blood pressure independent manner.