- 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.