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Mechanisms of endothelial dysfunction in penetrating cerebral arterioles of DOCA‐salt hypertensive rats
Author(s) -
Pires Paulo Wagner,
Matin Nusrat,
Garver Hannah,
Jackson William F,
Dorrance Anne McLaren
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.678.7
Subject(s) - myograph , medicine , acetylcholine , endocrinology , endothelial dysfunction , nitric oxide , vasodilation , endothelium , nitric oxide synthase , perfusion , contraction (grammar) , chemistry
Impaired endothelium‐dependent dilation is a hallmark of hypertension. Dilation of penetrating cerebral arterioles (PenA) is necessary to guarantee proper perfusion to regions of increased metabolism. Dysfunction of this system can lead to vascular dementia and Alzheimer's disease. The aim of this study was to understand the mechanisms of impaired dilation in PenA from deoxycorticosterone acetate (DOCA)‐salt hypertensive rats. Isolated PenA from DOCA and sham rats were mounted in a pressure myograph and endothelium‐dependent dilation was assessed with acetylcholine (Ach, 100μM, data shown as change in diameter from baseline). Data are means±SEM, n=5. PenA from DOCA‐salt rats dilated less to Ach. Nitric oxide synthase (NOS) inhibition with 10μM L‐NAME reduced Ach dilation in Sham but not in DOCA. Cyclooxygenase (COX) inhibition with 10μM indomethacin blunted Ach dilation in Sham but not in DOCA. These data suggest that hypertensive both uncoupling of NOS and increased COX activity play a role in endothelial dysfunction in DOCA‐salt hypertension.Sham DOCA p valueMyogenic Tone (%) 28±4 31±3 >;0.05 Ach 9.8±2.8μm 3.2±2.1μm <0.05 Ach+L‐NAME 10μM 6±1.7μm 8.8±1.3μm >;0.05 Ach+Indomethacin 10μM 5.4±1.5μm 10±2.4μm 0.09