Kompanowska-Jezierska E, Emmeluth C, Grove L, Christensen P, Sadowski J, Bie P
Department of Medical Physiology, The Panum Institute, University of Copenhagen, 2200 Copenhagen, Denmark.
Am J Physiol. 1998 Jun;274(6):R1619-25. doi: 10.1152/ajpregu.1998.274.6.R1619.
Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg . min-1 . kg body wt-1), plasma vasopressin concentration increased to 2.30 +/- 0.20 pg/ml compared with 0.12 +/- 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 +/- 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 +/- 15.8 micromol/min) than without vasopressin (4.6 +/- 0.4 ml/min and 14.4 +/- 4.1 micromol/min, respectively). Deamino-[Cys1,D-Arg8]vasopressin, a V2 receptor agonist (4 pg . min-1 . kg-1), mimicked the antidiuretic response (0.20 +/- 0.03 ml/min) without changing UNaV (9.7 +/- 4.4 micromol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 +/- 0.02 ml/min), and abolished the natriuresis (13.4 +/- 3.7 micromol/min). During AVP infusion, UNaV was highly correlated (r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.
在有意识的犬类进行伺服控制的水负荷过重（体重的2%）期间，研究了生理剂量血管加压素对肾脏的影响。在输注血管加压素（50 pg·min⁻¹·kg体重⁻¹）期间，血浆血管加压素浓度升至2.30±0.20 pg/ml，而对照期（水利尿）为0.12±0.03 pg/ml。输注血管加压素时，尿流显著降低（0.30±0.10 ml/min），钠排泄量（UNaV）显著升高（58.0±15.8 μmol/min），而未输注血管加压素时分别为4.6±0.4 ml/min和14.4±4.1 μmol/min。V2受体激动剂去氨基-[Cys1,D-Arg8]血管加压素（4 pg·min⁻¹·kg⁻¹）模拟了抗利尿反应（0.20±0.03 ml/min），但未改变UNaV（9.7±4.4 μmol/min）。在输注精氨酸血管加压素（AVP）期间给予吲哚美辛可抑制前列腺素E2排泄，增强抗利尿作用（0.10±0.02 ml/min），并消除利钠作用（13.4±3.7 μmol/min）。在输注AVP期间，UNaV与前列腺素E2排泄高度相关（r = 0.85）。所有组的血压、肾小球滤过率、血浆心钠素浓度以及近端小管重吸收率（由锂清除率得出）相似。数据表明，在犬类中，生理剂量的血管加压素可能通过激活非V2受体和肾脏内前列腺素的合成来诱导利钠作用。
