Düsing R, Bartter F C, Gill J R, Güllner H G, Lake C R
Prostaglandins. 1980 Dec;20(6):971-9. doi: 10.1016/0090-6980(80)90052-0.
The role of prostaglandins (PG) in the effects of potassium (K+)depletion was studied in six normal women. A mean K+-deficit of 220 mEq was induced with and without concomitant treatment with indomethacin (150 mg/day). Mean serum K+ concentration decreased from 4.2 +/- (S.E.) 0.1 to 3.2 +/- 0.1 mEq/L without indomethacin and from 4.1 +/- 0.1 to 3.2 +/- 0.1 mEq/L with indomethacin. "Supine" and "upright" plasma renin activity (PRA) and plasma norepinephrine concentration (NE) were unaltered by K+ -depletion alone but decreased with indomethacin. Plasma aldosterone (PA) was suppressed during K+-depletion (control: 7.2 +/- 2.6 ng/dl supine, 19.3 +/- 8.1 ng/dl upright; K+-depletion: 2.6 +/- 0.3 ng/dl supine, 5.5 +/- 1.3 ng/dl upright) and was paralleled by a decrease in urinary aldosterone. K+- depletion decreased urinary PGE2 from 667 +/- 133 to 343 +/- 60 ng/day (P less than 0.025) without a change in PGF2 alpha. The dose of exogenous angiotensin II (A II) which increased diastolic blood pressure by 20 mm Hg (pressor dose) was 7.1 +/- 1.4 ng/kg/min during control and increased to 11.0 +/- 0.7 ng/kg/min during K+-depletion (P less than 0.05). Indomethacin increased the sensitivity to A II both during control (pressor dose: 4.9 +/- 0.6 ng/kg/min) and K+ - depletion (pressor dose: 6.0 +/- 1.0 ng/kg/min). These results indicate that in healthy subjects, moderate short-term K+-depletion does not affect PRA or NE but decreases production of aldosterone and PGE2 by the kidney. The changes in vascular sensitivity to exogenous A II during K+-depletion and indomethacin and the decreases in plasma NE and PRA during indomethacin may be explained by changes in vascular vasodilator PG.
在六名正常女性中研究了前列腺素（PG）在钾（K +）缺乏效应中的作用。在使用和不使用消炎痛（150毫克/天）伴随治疗的情况下，诱导平均K +缺乏220毫当量。在不使用消炎痛时，平均血清K +浓度从4.2±（标准误）0.1降至3.2±0.1毫当量/升，使用消炎痛时从4.1±0.1降至3.2±0.1毫当量/升。单独的K +缺乏不会改变“仰卧”和“直立”状态下的血浆肾素活性（PRA）和血浆去甲肾上腺素浓度（NE），但消炎痛会使其降低。在K +缺乏期间，血浆醛固酮（PA）受到抑制（对照组：仰卧位7.2±2.6纳克/分升，直立位19.3±8.1纳克/分升；K +缺乏组：仰卧位2.6±0.3纳克/分升，直立位5.5±1.3纳克/分升），同时尿醛固酮也相应减少。K +缺乏使尿PGE2从667±133降至343±60纳克/天（P＜0.025），而PGF2α无变化。在对照组中，使舒张压升高20毫米汞柱的外源性血管紧张素II（A II）剂量（升压剂量）为7.1±1.4纳克/千克/分钟，在K +缺乏时升至11.0±0.7纳克/千克/分钟（P＜0.05）。消炎痛在对照组（升压剂量：4.9±0.6纳克/千克/分钟）和K +缺乏组（升压剂量：6.0±1.0纳克/千克/分钟）均增加了对A II的敏感性。这些结果表明，在健康受试者中，中度短期K +缺乏不影响PRA或NE，但会降低肾脏中醛固酮和PGE2的生成。K +缺乏和消炎痛期间血管对外源性A II敏感性的变化以及消炎痛期间血浆NE和PRA的降低可能由血管舒张性PG的变化来解释。
