Sokolova R I, Nekrasova A A, Levitskaia Iu V, Speranskaia N V, Volkov V N
Kardiologiia. 1977 Oct;17(10):78-85.
Chronic administration of small doses of prostaglandin-synthesis inhibitor indometacin against the background of a salt load or unilateral nephrectomy induces the development of arterial hypertension in rats. Arterial pressure increases (two fold on the average) on the 6th week of the experiment in 60-80% of the animals. Arterial hypertension developing against the background of a salt load is marked by retention of sodium in the organism and increase the intravascular volume, while that developing in unilateral nephrectomy--by increased sodium excretion and reduced intravascular volume. Depressed activity of the renin-angiotensin-aldosterone system and conspicious changes in the renal vascular channel are noted in both forms of arterial hypertension. It is assumed that disorders in the metabolism of cyclic nucleotides underlie the changes occurring in the renal vessels due to the effect of indometacin. Similar generalized changes in the peripheral vascular channel on the whole may be the cause of the increased vascular resistance and one of the causative factors of the hypertension development.
在盐负荷或单侧肾切除背景下长期给予小剂量前列腺素合成抑制剂吲哚美辛会诱发大鼠动脉高血压。在实验的第6周，60 - 80%的动物动脉血压升高（平均升高两倍）。在盐负荷背景下发生的动脉高血压的特征是机体钠潴留和血管内容量增加，而在单侧肾切除背景下发生的动脉高血压则表现为钠排泄增加和血管内容量减少。在两种形式的动脉高血压中均观察到肾素 - 血管紧张素 - 醛固酮系统活性降低以及肾血管通道的明显变化。据推测，由于吲哚美辛的作用，肾血管中发生的变化是以环核苷酸代谢紊乱为基础的。总体而言，外周血管通道的类似全身性变化可能是血管阻力增加的原因，也是高血压发生的致病因素之一。
