{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T22:13:17Z","timestamp":1791238397626,"version":"4.1.0"},"reference-count":31,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2007,4]]},"abstract":"<jats:p> Deoxycorticosterone acetate (DOCA)-salt hypertension has an important endothelin-1 (ET-1)-dependent component. ET-1-induced vascular damage may be mediated in part by oxidative stress and vascular inflammation. Homozygous osteopetrotic ( Op\/Op) mice, deficient in macrophage colony-stimulating factor (m-CSF), exhibit reduced inflammation. We investigated in osteopetrotic ( Op\/Op) mice the effects of DOCA-salt hypertension on vascular structure, function, and oxidative stress, the latter as manifested by reduced nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase activity. Mice were implanted with DOCA (200 mg\/mouse, under 5% isofluorane anesthesia) and given saline for 14 days. Systolic blood pressure (mmHg) was significantly increased (146 \u00b1 2 and 138 \u00b1 1; P &lt; 0.001 vs. basal 115 \u00b1 3 and 115 \u00b1 3, respectively) by DOCA-salt in wild-type (+\/+) and heterozygous ( Op\/+) mice, but not in Op\/Op mice (130 \u00b1 1 vs. basal 125 \u00b1 3). Norepinephrine contractile response was significantly enhanced, while acetylcholine endothelium-dependent vasodilation was significantly impaired in DOCA-salt-treated +\/+ and Op\/+ mice compared with control mice. No changes in norepinephrine-induced contraction and acetylcholine-induced relaxation were observed in DOCA-salt Op\/Op mice. DOCA-salt +\/+ and Op\/+ mice had significantly increased mesenteric resistance artery media-to-lumen ratio and media cross-sectional area, neither of which were altered in Op\/Op mice. Basal vascular superoxide production and NAD(P)H oxidase activity, vascular cell adhesion molecule-1 expression, and macrophage infiltration were significantly increased only in DOCA-salt +\/+ mice. Thus m-CSF-deficient mice developed less endothelial dysfunction, vascular remodeling, and oxidative stress induced by DOCA-salt than +\/+ and Op\/+ mice, suggesting that inflammation may play a role in DOCA-salt hypertension, a model that results in part from effects of ET-1, which has proinflammatory actions. <\/jats:p>","DOI":"10.1152\/ajpheart.01118.2006","type":"journal-article","created":{"date-parts":[[2006,12,1]],"date-time":"2006-12-01T20:34:25Z","timestamp":1165005265000},"page":"H1789-H1795","source":"Crossref","is-referenced-by-count":118,"title":["Resistance artery remodeling in deoxycorticosterone acetate-salt hypertension is dependent on vascular inflammation: evidence from m-CSF-deficient mice"],"prefix":"10.1152","volume":"292","author":[{"given":"Eun 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