Nakamura T, Sakamaki T, Kurashina T, Hoshino J, Sato K, Ono Z, Murata K
Second Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.
Life Sci. 1994;55(4):PL67-72. doi: 10.1016/0024-3205(94)00736-5.
Our objective was to assess the effect of endogenous AVP on renal hemodynamics and excretory function. We measured mean arterial pressure (MAP), renal blood flow (RBF), glomerular filtration rate (GFR) and urine osmolality before and after the intravenous infusion of a V1 antagonist (OPC-21268), a V2 antagonist (OPC-31260) and their vehicle (saline) in anesthetized male Wistar rats. The infusion of the V2 antagonist increased the urine flow rate and reduced the urine osmolality significantly (p < 0.05). The infusion of saline and the V1 antagonist did not change the urine flow rate or the urine osmolality. The infusion of saline, the V1 antagonist and the V2 antagonist had no effect on MAP, RBF or GFR. These results suggest that endogenous AVP plays a critical role in the regulation of renal water reabsorption mediated through the V2 receptor.
我们的目的是评估内源性血管加压素（AVP）对肾血流动力学和排泄功能的影响。我们在麻醉的雄性Wistar大鼠中静脉输注V1拮抗剂（OPC - 21268）、V2拮抗剂（OPC - 31260）及其溶媒（生理盐水）前后，测量了平均动脉压（MAP）、肾血流量（RBF）、肾小球滤过率（GFR）和尿渗透压。输注V2拮抗剂显著增加了尿流率并降低了尿渗透压（p < 0.05）。输注生理盐水和V1拮抗剂未改变尿流率或尿渗透压。输注生理盐水、V1拮抗剂和V2拮抗剂对MAP、RBF或GFR均无影响。这些结果表明，内源性AVP在通过V2受体介导的肾水重吸收调节中起关键作用。
