Zipser R D, Little T E, Wilson W, Duke R
J Clin Endocrinol Metab. 1981 Sep;53(3):522-6. doi: 10.1210/jcem-53-3-522.
To evaluate the relationship of renal prostaglandin synthesis to urine-concentrating mechanisms, 14 healthy subjects received antidiuretic hormone (ADH) and the nonpressor ADH analog desamino-d-arginine vasopressin (dD'AVP). Endogenous ADH was increased by water deprivation. Urinary prostaglandin E2 (PGE2) was measured by RIA and by bioassay. ADH, dD'AVP, and dehydration each reduced urinary volume by a similar amount (from 582 +/- 66 to an average of 141 +/- 13 ml/4 h) and similarly increased osmolality (from 231 +/- 13 to 721 +/- 31 mosmol/kg). Dehydration and dD'AVP reduced PGE2 from 44 +/- 4 to 25 +/- 5 and 30 +/- 5 ng/4 h, respectively (P less than 0.01), suggesting an inverse correlation of PGE2 with urine osmolality (r = -0.48; P less than 0.005). In contrast, ADH increased urinary PGE2 to 102 +/- 23 ng/4 h (P less than 0.02). Infusions of another vasoconstrictor peptide, angiotensin II, to six of the subjects doubled urine osmolality and also increased urinary PGE2 excretion. These data do not support the theory that the antidiuretic effect of ADH enhances PG synthesis; instead, the data indicate that ADH has two effects on PGE2 excretion: 1) stimulation, presumably by pharmacological pressor activity, and 2) inhibition by antidiuresis.
为评估肾脏前列腺素合成与尿液浓缩机制之间的关系，14名健康受试者接受了抗利尿激素（ADH）和非加压性ADH类似物去氨基 - d - 精氨酸血管加压素（dD'AVP）。通过限水增加内源性ADH。采用放射免疫分析法（RIA）和生物测定法测定尿前列腺素E2（PGE2）。ADH、dD'AVP和脱水均使尿量减少相似量（从582±66降至平均141±13 ml/4 h），并使渗透压相似地升高（从231±13升至721±31 mosmol/kg）。脱水和dD'AVP分别使PGE2从44±4降至25±5和30±5 ng/4 h（P<0.01），提示PGE2与尿渗透压呈负相关（r = -0.48；P<0.005）。相反，ADH使尿PGE2增加至102±23 ng/4 h（P<0.02）。给其中6名受试者输注另一种血管收缩肽血管紧张素II，使尿渗透压加倍，同时也增加了尿PGE2排泄。这些数据不支持ADH的抗利尿作用增强前列腺素合成的理论；相反，数据表明ADH对PGE2排泄有两种作用：1）刺激作用，可能是通过药理加压活性，2）通过抗利尿作用产生抑制作用。
