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MYLOID DIFFERENTIATION FACTOR 88 (MYD88) DOES NOT CONTRIBUTE TO HYPERTENSION OR ENDOTHELIAL DYSFUNCTION PRODUCED BY ANGIOTENSIN II
Author(s) -
Gomolak Jessica R,
Faulkner Jessica L,
Didion Sean P
Publication year - 2013
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.27.1_supplement.1131.15
Subject(s) - angiotensin ii , endothelial dysfunction , medicine , endocrinology , renin–angiotensin system , endothelium , blood pressure , innate immune system , receptor , pathophysiology of hypertension , carotid arteries
Although a role for adaptive immunity has begun to emerge in hypertension, much less is known regarding the potential role of innate immunity in hypertension. The goal of this study was to test the hypothesis that deficiency of MyD88 (a key mediator of toll‐like receptor signaling) limits the development of hypertension and endothelial dysfunction produced by Angiotensin II (Ang II). Blood pressure (BP) and vascular responses were examined in wild‐type (WT) and MyD88‐deficient (MyD88−/−) mice infused with Ang II (1000 ng/kg/min via osmotic minipump for 14 Days). Ang II produced a similar degree (P>;0.05) of hypertension and cardiac hypertrophy in WT and MyD88−/− mice. Ang II infusion was associated with endothelial dysfunction in carotid arteries from Ang II‐infused WT and MyD88−/− mice as compared to their respective controls (p<0.01). Ang II produced a similar degree of endothelial dysfunction in carotid arteries from WT and MyD88−/− mice. Contractile responses to U46619 were similar in all groups. Contrary to our hypothesis, these data suggest that MyD88, a major component of innate immune signaling, does not contribute to the hypertension or endothelial dysfunction produced by Ang II. Supported by NIH HL‐089884 & HL‐107632.