著者
大塚 雄司 原澤 信介 杉浦 仁 小池 美由紀 秋元 秀郎 石井 利明 阿部田 ひろみ 岡部 龍也 久代 登志男 上松瀬 勝男
出版者
Japanese Society of Nephrology
雑誌
日本腎臓学会誌 (ISSN:03852385)
巻号頁・発行日
vol.42, no.8, pp.619-624, 2000

Previous studies have shown that hypertension causes endothelial dysfunction. To study the influence of exogenous nitric oxide (NO) on endothelial dysfunction produced by hypertension, we administered a non-depressor dose of nipradilol to two-kidney, one clip renovascular hypertensive rats (2K1C). Sprague-Dawley rats underwent either sham surgery (G-l) or clipping of the left renal artery. From day seven, 2K1C were randomized into 3 groups, placebo treatment (G-2), nipradilol treament (G-3, ) and propranolol treatment (G-4). Urinary NO<SUP>-</SUP><SUB>2</SUB> +N0<SUP>-</SUP><SUB>3</SUB> (NOx) excretion (UNOxV) was measured 4 weeks after clipping, and then, acetylcholine (Ach), A23187, or sodium nitroprusside (SNP) -induced relaxation were measured in the aorta. Blood pressure was increased in G-2, G-3, and G-4 compared to G-1. UNOxV was lower in G-2, G-3, and G-4 compared to G-1, but UNOxV was higher in G-3 compared to G-2 and G-4. Although Ach or A23187-induced relaxation was significantly decreased in isolated artery from G-2, G-3, and G-4 compared with those from G-1. Ach- or A23187-induced relaxation was improved in G-3. SNP induced relaxation did not differ among the 4 groups. These results suggest that exogenous NO from nipradilol reduces the endothelial dysfunction caused by hypertension without changing the blood pressure.

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こんな論文どうですか? Two‐kidney,one‐clip腎血管性高血圧ラットにおける血管内皮機能障害に及ぼす外因性一酸化窒素の影響(大塚 雄司ほか),2000 https://t.co/hoMY4jc97r

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