速尿导致人体游离花生四烯酸增加是前列腺素和肾素释放的原因。
Increase of free arachidonic acid by furosemide in man as the cause of prostaglandin and renin release.
作者信息
Weber P C, Scherer B, Larsson C
出版信息
Eur J Pharmacol. 1977 Feb 7;41(3):329-32. doi: 10.1016/0014-2999(77)90326-0.
Arachidonic acid (C20 :4) plasma renin activity (PRA), PGF2alpha, and sodium excretion were determined before and after furosemide in men. C20 : 4 and PRA increase (p less than 0.005) within 10 min after furosemide, PRA then decreased again whereas C20 : 4 levels remained elevated. Maximal exretion of PGF2alpha and sodium occurred 30-60 min after furosemide. Indomethacin prevented the rise of C20 : 4, PRA and PGF2alpha after furosemide, leaving sodium excretion unaltered. The release of C20 : 4 is assumed to be the primary mechanism of furosemide to increase PG biosynthesis and renin release.
在男性中测定了速尿给药前后的花生四烯酸（C20 :4）、血浆肾素活性（PRA）、前列腺素F2α（PGF2α）和钠排泄量。速尿给药后10分钟内，C20 : 4和PRA升高（p<0.005），随后PRA再次下降，而C20 : 4水平仍保持升高。PGF2α和钠的最大排泄量出现在速尿给药后30 - 60分钟。消炎痛可阻止速尿给药后C20 : 4、PRA和PGF2α的升高，而钠排泄量不变。C20 : 4的释放被认为是速尿增加前列腺素生物合成和肾素释放的主要机制。
Zotero 插件