Düsing R, Scherhag R, Tippelmann R, Budde U, Glänzer K, Kramer H J
J Biol Chem. 1982 Feb 25;257(4):1993-6.
Slices of rat aorta were incubated in Krebs-Ringer bicarbonate buffer for measurements of immunoreactive 6-ketoprostaglandin F1 alpha, thromboxane (TX) B2, prostaglandin (PG)E2, and PGF2 alpha, and in Tris buffer (pH 9.3) for determination of prostacyclin (PGI2)-like activity. No significant generation of TXB2, PGE2, or PGF2 alpha by rat aortic tissue could be detected. The time-dependent release of 6-keto-PGF1 alpha Krebs-Ringer bicarbonate buffer closely correlated with PGI2 generation in alkaline Tris buffer. During a 30-min incubation period, 6-keto-PGF1 alpha, release was 79.8 +/- 3.3 pmol/mg at a buffer potassium concentration of 3.9 mmol/liter and significantly increased by 23% to 98.3 +/- 8.5 pmol/mg (P less than 0.025) in the absence of potassium in the incubation medium. A smaller decrease in buffer potassium concentration to 2.1 mmol/liter and an increase to 8.8 mmol/liter did not significantly alter aortic 6-keto-PGF1 alpha release. Changes in the incubation buffer sodium concentration from 144 mmol/liter to either 138 or 150 mmol/liter at a constant potassium concentration of 3.9 mmol/liter did not alter the recovery of 6-keto-PGF1 alpha. Our results support the concept that PGI2 is the predominant product of arachidonic acid metabolism in rat aorta. They further show that PGI2 can be recovered quantitatively as 6-keto-PGF1 alpha under the present in vitro conditions. In addition, this in vitro study points to the potassium ion as a modulator of vascular PGI2 synthesis with a stimulation at low potassium concentrations.
将大鼠主动脉切片置于 Krebs-Ringer 碳酸氢盐缓冲液中，用于测量免疫反应性 6-酮前列环素 F1α、血栓素（TX）B2、前列腺素（PG）E2 和 PGF2α；置于 Tris 缓冲液（pH 9.3）中，用于测定前列环素（PGI2）样活性。未检测到大鼠主动脉组织产生显著量的 TXB2、PGE2 或 PGF2α。在 Krebs-Ringer 碳酸氢盐缓冲液中，6-酮-PGF1α 的时间依赖性释放与碱性 Tris 缓冲液中 PGI2 的生成密切相关。在 30 分钟的孵育期内，缓冲液钾浓度为 3.9 mmol/升时，6-酮-PGF1α 的释放量为 79.8±3.3 pmol/mg，而在孵育介质中无钾的情况下，释放量显著增加 23%，达到 98.3±8.5 pmol/mg（P＜0.025）。缓冲液钾浓度较小幅度降至 2.1 mmol/升和升至 8.8 mmol/升，并未显著改变主动脉 6-酮-PGF1α 的释放。在钾浓度恒定为 3.9 mmol/升的情况下，将孵育缓冲液钠浓度从 144 mmol/升变为 138 或 150 mmol/升，并未改变 6-酮-PGF1α 的回收率。我们的结果支持这样的概念，即 PGI2 是大鼠主动脉中花生四烯酸代谢的主要产物。它们进一步表明，在目前的体外条件下，PGI2 可以定量回收为 6-酮-PGF1α。此外，这项体外研究指出钾离子是血管 PGI2 合成的调节剂，在低钾浓度下具有刺激作用。
