Stimulation of rabbit renal PGE2 biosynthesis by dietary sodium restriction.
Stimulation of rabbit renal PGE2 biosynthesis by dietary sodium restriction.
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通过限制饮食钠刺激兔肾 PGE2 生物合成。
DOI：
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发表时间：
1979
影响因子：
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通讯作者：
J. B. Lee
中科院分区：
文献类型：
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作者：
R. Stahl;A. Attallah;D. Bloch;J. B. Lee
在Krebs-Ringer HCO3缓冲液中，测定低钠(LS)、正常钠(NS)和高钠(HS)饲料孵育30min前后兔肾乳头(P)、外髓(OM)和皮质(C)切片中前列腺素E_2(PGE_2)的免疫反应。在孵化前10天每天测量24小时尿PGE2。LS日尿PGE2显著升高(911+/-54 ng)，NS组降至605+/-33 ng，HS组为558+/-48 ng，P组最高(35.5+/-5.1微克/g，5.1微克/g)，NS组降至16.9+/-1.3，HS组为18.0+/-2.6微克/g。在OM和C中也观察到了类似的模式，但数量要低得多。PGE2生物合成以LS最高(P，139+/-21；OM，58.8+/-5.1；C，0.20+/-0.05微克·g-1.30min-1)，HS最低(P，58.9+/-7.4；OM，11.8+/-3.1；C，0.07+/-0.01微克·g-1.30min-1)。尽管P组的PGE_2浓度高于OM组，但LS组OM-PGE_2生物合成的百分率是P组的3-4倍。由于OM组为28%，P组为2%，这些结果表明LS显著刺激PGE_2的生物合成，主要在OM组，而P组和C组较少，提示OM-PGE_2在肾脏对钠缺乏的适应中起重要作用。
Immunoreactive prostaglandin E2 (PGE2) was measured in slices of renal papilla (P), outer medulla (OM), and cortex (C) before and after 30 min of incubation (biosynthesis) in Krebs-Ringer HCO3- buffer in rabbits on low (LS), normal (NS), and high (HS) sodium diets. The 24-h urine PGE2 was also measured daily for 10 days prior to incubation. Daily urine PGE2 was significantly higher (911 +/- 54 ng) in LS, decreasing to 605 +/- 33 at NS, and 558 +/- 48 ng at HS, Initial slice PGE2 was highest in P at LS (35.5 +/- 5.1 MICROGRAMS/G), 5.1 microgram/g), decreasing to 16.9 +/- 1.3 at NS and 18.0 +/- 2.6 micrograms/g at HS. Similar patterns were observed in OM and C, which were quantitatively much lower. PGE2 biosynthesis was highest at LS (P, 139 +/- 21; OM, 58.8 +/- 5.1; C, 0.20 +/- 0.05 micrograms.G-1.30 Min-1) and lowest at HS (P, 58.9 +/- 7.4; OM, 11.8 +/- 3.1; C, 0.07 +/- 0.01 micrograms.g-1.30 min-1). Although PGE2 concentration was higher in P than in OM, the percent increase in OM PGE2 biosynthesis on LS was 3--4 times greater than in P. Since OM is 28% and P is 2% of total renal mass, these results indicate that LS markedly stimulates PGE2 biosynthesis primarily in OM and to a lesser extent in P and C, findings suggesting an important role for OM PGE2 in the renal adaptation to sodium deprivation.