Sokolova R I, Vikhert A M, Nekrasova A A, Volkov V N, Zharova E A
Kardiologiia. 1978 Feb;18(2):110-4.
Arterial hypertension was induced in experiments on rats by chronic injection of indometacin, an inhibitor of prostaglandin synthesis, combined with a salt load or unilateral nephrectomy. A twofold rise in arterial pressure, on average, was noted at the end of the 6th week of the inhibitor injection. The development of arterial hypertension following indometacin injection and a salt load led to reduced excretion of sodium and water, increased intravascular volume, and increased sodium content in the aortic wall. In the group of nephrectomized and indometacin treated animals, on the contrary, sodium and water excretion increased, intravascular volume diminished, and the content of sodium in the aortic wall decreased. Chronic injection of indometacin alone into intact animals did not lead to a rise of arterial pressure within the same periods of time and did not induce changes in the renal excretory function. It is presumed that disorder of water-salt homeostasis is one of the mechanisms of the increase in arterial pressure.
通过长期注射消炎痛（一种前列腺素合成抑制剂）并结合盐负荷或单侧肾切除，在大鼠实验中诱发动脉高血压。在注射抑制剂第6周结束时，平均动脉压升高了两倍。注射消炎痛并给予盐负荷后动脉高血压的发展导致钠和水排泄减少、血管内容量增加以及主动脉壁钠含量增加。相反，在肾切除并接受消炎痛治疗的动物组中，钠和水排泄增加，血管内容量减少，主动脉壁钠含量降低。在相同时间段内，单独对完整动物长期注射消炎痛不会导致动脉压升高，也不会引起肾排泄功能改变。据推测，水盐稳态紊乱是动脉压升高的机制之一。
