Bojesen E, Bojesen I N
Institute of Experimental Hormone Research, University of Copenhagen, Panum Institute, Denmark.
Acta Endocrinol (Copenh). 1989 Apr;120(4):459-65. doi: 10.1530/acta.0.1200459.
Brattleboro rats with hereditary diabetes insipidus make it possible to investigate effects of the urea concentration on the in vitro and in vivo production of prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha) by the renal papilla independently of any vasopressin effects. The rates of prostaglandin production in vitro are increasing between 100 and 1030 mmol/l urea and decreasing above 1030 mmol/l. The ratio PGE2/PGF2 alpha remains constant at about 4. Normally hydrated and 24 h water-deprived animals in steady state of urine formation were compared in vivo. Urine osmolality increased from 167 +/- 6 (N = 5) to 1113 +/- 35 (N = 15) mosmol/kg water and papillary urea concentration from 50 +/- 7 to 304 +/- 19 mmol/l after water deprivation. Urinary excretion rates of PGF2 alpha increased from 0.83 +/- 0.12 to 3.80 +/- 0.37 ng/h. The excretion of PGE2 was unaffected. PGE2 + PGF2 alpha excretion rates increased from 1.62 +/- 0.25 to 4.61 +/- 0.42 ng/h. These values are in accordance with values predicted from work with Sprague-Dawley rats. Together with previously published data on Sprague-Dawley rats these results indicate that variations of prostaglandin production in the conscious rat in steady state of urine formation can be accounted for by variations of plasma vasopressin and of papillary urea concentration. Variations in the excretion fraction are due to other causes.
遗传性尿崩症的布拉德福德大鼠使得在独立于任何抗利尿激素作用的情况下,研究尿素浓度对肾乳头体外和体内前列腺素E2和F2α(PGE2和PGF2α)生成的影响成为可能。体外前列腺素生成速率在尿素浓度为100至1030 mmol/l之间增加,而在高于1030 mmol/l时降低。PGE2/PGF2α比值保持恒定在约4。对处于尿液生成稳态的正常水合和24小时缺水动物进行了体内比较。缺水后,尿渗透压从167±6(N = 5)升至1113±35(N = 15)mosmol/kg水,乳头尿素浓度从50±7升至304±19 mmol/l。PGF2α的尿排泄率从0.83±0.12增至3.80±0.37 ng/h。PGE2的排泄未受影响。PGE2 + PGF2α排泄率从1.62±0.25增至4.61±0.42 ng/h。这些值与用斯普拉格 - 道利大鼠实验预测的值一致。连同先前发表的关于斯普拉格 - 道利大鼠的数据,这些结果表明,在尿液生成稳态的清醒大鼠中,前列腺素生成的变化可由血浆抗利尿激素和乳头尿素浓度的变化来解释。排泄分数的变化是由其他原因引起的。