Oestrogen lowers the plasma osmotic threshold for arginine vasopressin (AVP) release but without commensurate changes in renal concentrating response, suggesting oestrogen (OE2) may lower renal sensitivity to AVP. Ten women (23 ± 1 years) received a gonadotropin releasing hormone analogue (GnRHa), leuprolide acetate, to suppress OE2 for 35 days, and then added OE2 (two patches each delivering 0.1 mg day−1) on days 32–35. On days 28 and 35 we tested blood and renal water and sodium (Na+) regulation during stepwise 60 min AVP infusions (10, 35, 100, 150 and 200 μu (kg body weight)−1 Pitressin). Plasma OE2 concentration increased from 19 ± 4 to 152 ± 3 pg ml−1 and plasma progesterone concentration was unchanged (1.0 ± 0.4 and 0.7 ± 0.1 ng ml−1) for GnRHa and OE2 administration, respectively. Standard log plots of plasma AVP concentration ([AVP]P) vs. urine osmolality (OsmU) were fitted to a sigmoidal curve, and EC50 was determined by non-linear regression curve fitting of concentration-response data. OsmU rose exponentially during AVP infusions, but hormone treatments did not affect EC50 (3.3 ± 0.07 and 3.1 ± 0.6 pg ml−1, for GnRHa and OE2, respectively). However, the urine osmolality increase was greater within the physiological range (˜2.5−3.4 pg ml−1[AVP]P) during OE2 treatment. Throughout most of the AVP infusion, the rate of clearance of AVP from plasma (PCRAVP) was increased during OE2 (45.5 ml (kg body weight)−1 min−1) compared to GnRHa administration (33.1 ml (kg body weight)−1 min−1; mean for the 100–200 μu (kg body weight)−1 infusion rates). The rate of renal free water clearance (CH2O) was similar between hormone treatments. Sodium excretion fell during OE2 administration due to greater distal tubular sodium reabsorption. Despite more rapid PCRAVP, renal concentrating response to graded AVP infusions was unaffected by oestrogen treatment suggesting oestrogen does not affect overall renal sensitivity to AVP. However, OE2 may increase renal fluid retention within a physiological range of AVP.
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机译：雌激素可降低精氨酸加压素（AVP）释放的血浆渗透压阈值，但肾浓缩反应没有相应的变化，表明雌激素（OE2）可能会降低肾脏对AVP的敏感性。十名妇女（23±1岁）接受促性腺激素释放激素类似物（GnRHa）醋酸亮丙瑞林抑制OE2达35天，然后添加OE2（两个贴片，每片释放0.1 mg day -1 ）在第32-35天。在第28天和第35天，我们在逐步输注60分钟AVP（10、35、100、150和200μu（kg体重）的过程中测试了血液，肾脏水和钠（Na + ）调节-1 Pitressin）。血浆OE2浓度从19±4 pg增加到152±3 pg ml -1 ，血浆孕酮浓度保持不变（1.0±0.4和0.7±0.1 ng ml -1 ） GnRHa和OE2管理。将血浆AVP浓度（[AVP] P）与尿渗透压（OsmU）的标准对数图拟合为S形曲线，并通过浓度-响应数据的非线性回归曲线拟合确定EC50。在AVP输注期间，OsmU呈指数增长，但激素治疗并没有影响EC50（GnRHa和OE2分别为3.3±0.07和3.1±0.6 pg ml -1 ）。然而，在OE2治疗期间，在生理范围内（〜2.5-3.4 pg ml -1 [AVP] P），尿渗透压的增加更大。在大多数AVP输注中，OE2期间血浆（AVP）清除率（PCRAVP）有所增加（45.5 ml（kg体重） -1 min -1 ）与GnRHa给药相比（33.1 ml（kg体重） -1 min -1 ；平均值为100–200μu（kg体重） -1 < / sup>输注速率）。激素治疗之间的肾游离水清除率（CH 2O ）相似。 OE 2 给药期间，由于远端肾小管钠吸收增加，钠排泄下降。尽管PCR AVP 的速度更快，但雌激素治疗并未影响对分级AVP输注的肾脏浓缩反应，这表明雌激素不会影响总体肾脏对AVP的敏感性。然而，OE 2 可能在AVP的生理范围内增加肾液fluid留。
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