Rodionov Iu Ia, Rodionov V Ia, Matsuganova T N
Kardiologiia. 1977 Oct;17(10):89-92.
Experiments were conducted on 119 male and female mongrel/albino rats and on 5 male rabbits to study the mechanisms of the in vivo effect of the inhibitors of the biosynthesis of prostaglandins, acetylsalicylic acid, and indometacin, taking into account the previously obtained data on the fact that these inhibitors elevate mean arterial pressure and increase vasopressor sensitivity to adrenalin and noradrenaline in experimental animals. It was found that these inhibitors of prostaglandin biosynthesis promote the development of "salt hypertension" in rats against the background of a noticeable increase in vasopressor sensitivity to catecholamines. Intravenous administration to rabbits of angiotensin-11 in pressor doses causes an increase in the content of group E prostaglandins in the blood plasma of rabbits and a decrease in the renin activity ("feedback" effect). The data obtained have confirmed the assumption that prostaglandins take part in the arterial pressure control and suggested that in exhaustion or hereditary deficiency of the function of the prostaglandin production system the vessels may escape the depressor control, in this case the sensitivity to pressor factors increase and stable arterial hypertension develops.
以119只雄性和雌性杂种/白化大鼠以及5只雄性兔子为实验对象，研究前列腺素生物合成抑制剂、乙酰水杨酸和吲哚美辛的体内作用机制，同时考虑到先前获得的关于这些抑制剂会提高实验动物平均动脉压以及增强对肾上腺素和去甲肾上腺素的血管升压敏感性的数据。研究发现，这些前列腺素生物合成抑制剂在对儿茶酚胺的血管升压敏感性显著增加的背景下，会促使大鼠发生“盐性高血压”。以升压剂量给兔子静脉注射血管紧张素II，会导致兔子血浆中E组前列腺素含量增加，肾素活性降低（“反馈”效应）。所获数据证实了前列腺素参与动脉血压调节的假设，并表明在前列腺素产生系统功能耗竭或遗传性缺陷的情况下，血管可能逃避降压控制，此时对升压因子的敏感性增加，进而发展为持续性动脉高血压。
