前列腺素作为海蟾蜍膀胱酸化的介质。
Prostaglandins as mediators of acidification in the urinary bladder of Bufo marinus.
作者信息
Frazier L W, Yorio T
机构信息
Department of Physiology, Baylor College of Dentistry, Dallas, Texas 75246.
出版信息
Proc Soc Exp Biol Med. 1990 May;194(1):10-5. doi: 10.3181/00379727-194-43046.
Experiments were performed to determine whether prostaglandins (PG) play a role in H+ and NH4+ excretion in the urinary bladder of Bufo marinus. Ten paired hemibladders from normal toads were mounted in chambers. One was control and the other hemibladder received PGE2 in the serosal medium (10(-5) M). H+ excretion was measured by change in pH in the mucosal fluid and reported in units of nmol (100 mg tissue)-1 (min)-1. NH4+ excretion was measured colorimetrically and reported in the same units. The control group H+ excretion was 8.4 +/- 1.67, while the experimental group was 16.3 +/- 2.64 (P less than 0.01). The NH4+ excretion in the experimental and control group was not significantly different. Bladders from toads in a 48-hr NH4+Cl acidosis (metabolic) did not demonstrate this response to PGE2 (P greater than 0.30). Toads were put in metabolic acidosis by gavaging with 10 ml of 120 mM NH4+Cl 3 x day for 2 days. In another experiment, we measured levels of PG in bladders from control (N) and animals placed in metabolic acidosis (MA). Bladders were removed from the respective toad, homogenized, extracted, and PG separated using high-pressure liquid chromatography and quantified against PG standards. The results are reported in ng (mg tissue)-1. PGE2 fraction in N was 1.09 +/- 0.14 and in MA was 3.21 +/- 0.63 (P less than 0.01). PGF1 alpha, F2 alpha and I2 were not significantly different in N and MA toads. Bladders were also removed from N and MA toads, and incubated in Ringer's solution containing [3H]arachidonic acid (0.2 microCi/ml) at 25 degrees C for 2 hr. Bladders were then extracted for PG and the extracts separated by thin layer chromatography. PG were identified using standards and autoradiography, scraped from plates, and counted in a scintillation detector. The results are reported in cpm/mg tissue x hr +/- SEM. In MA toads, PG6-keto-F1 alpha = 1964 +/- 342, PGF2 alpha = 1016 +/- 228, and PGE2 = 904 +/- 188; in N animals PG6-keto-F1 alpha = 625 +/- 280, PGF2 alpha = 364 +/- 85, and PGE2 = 404 +/- 104; (P less than 0.01, less than 0.025, less than 0.05, respectively). We conclude that PGE2 may be an important mediator of H+ excretion in toad urinary bladder and that endogenous PGE2 levels are increased in response to MA.
进行实验以确定前列腺素（PG）是否在海蟾蜍膀胱中H⁺和NH₄⁺排泄中发挥作用。从正常蟾蜍获取10对半膀胱并安装在腔室中。一个作为对照，另一个半膀胱在浆膜介质中接受前列腺素E₂（PGE₂，10⁻⁵ M）。通过黏膜液pH变化测量H⁺排泄，以nmol（100 mg组织）⁻¹（分钟）⁻¹为单位报告。通过比色法测量NH₄⁺排泄，并以相同单位报告。对照组H⁺排泄量为8.4±1.67，而实验组为16.3±2.64（P＜0.01）。实验组和对照组的NH₄⁺排泄量无显著差异。处于48小时NH₄⁺Cl酸中毒（代谢性）的蟾蜍的膀胱对PGE₂未表现出这种反应（P＞0.30）。通过每天3次灌胃10 ml 120 mM NH₄⁺Cl，持续2天使蟾蜍处于代谢性酸中毒状态。在另一项实验中，我们测量了对照（N）蟾蜍和处于代谢性酸中毒（MA）的动物膀胱中的PG水平。从相应蟾蜍取出膀胱，匀浆、提取，使用高压液相色谱分离PG并根据PG标准品进行定量。结果以ng（mg组织）⁻¹报告。N组中PGE₂含量为1.09±0.14，MA组为3.21±0.63（P＜0.01）。N组和MA组蟾蜍中PGF1α、F2α和I2无显著差异。还从N组和MA组蟾蜍取出膀胱，在含[³H]花生四烯酸（0.2 μCi/ml）的林格氏液中于25℃孵育2小时。然后提取膀胱中的PG，提取物通过薄层色谱分离。使用标准品和放射自显影鉴定PG，从板上刮下并在闪烁探测器中计数。结果以cpm/mg组织×小时±标准误报告。在MA组蟾蜍中，PG6 - 酮 - F1α = 1964±342，PGF2α = 1016±228，PGE₂ = 904±188；在N组动物中，PG6 - 酮 - F1α = 625±280，PGF2α = 364±85，PGE₂ = 404±104；（分别为P＜0.01、＜0.025、＜0.05）。我们得出结论，PGE₂可能是蟾蜍膀胱中H⁺排泄的重要介质，并且内源性PGE₂水平会因代谢性酸中毒而升高。
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