Klembovskiĭ A A, Nekrasova A A, Shkhvatsabaia I K
Kardiologiia. 1984 May;24(5):84-8.
The state of the renal prostaglandins (PG) system was assessed in 54 patients with essential hypertension, stage IB-IIA, as compared to that of patients with symptomatic arterial hypertensions. A decrease in renal PGE2 production, noted in all hypertensive patients and determined on the basis of its diurnal excretion, was particularly pronounced in essential hypertension. Diurnal PGE2 excretion decreased as hypertension progressed in patients with essential hypertension, and renal PGF2 alpha production became prevalent. Renal function is dependent on the level of PG production by the kidney. As renal concentration capacity decreases and renographic findings become less satisfactory, PGE2 excretion decreases as well. Salt loads can bring out functional insufficiency of the renal PG system in essential hypertension, as reflected in a much smaller increase in PGE2 excretion, as compared to the control values, at early stages of salt loading and a considerable increase in PGF2 alpha excretion. In essential hypertension, inadequate renal prostaglandin response to salt loading is, to a certain degree, related to changed renal PGE-9-ketoreductase activity.
对54例IB-IIA期原发性高血压患者的肾脏前列腺素（PG）系统状态进行了评估，并与症状性动脉高血压患者进行了比较。在所有高血压患者中均观察到肾脏PGE2生成减少，这是根据其昼夜排泄量确定的，在原发性高血压中尤为明显。在原发性高血压患者中，随着高血压病情进展，PGE2的昼夜排泄量减少，且肾脏PGF2α生成占优势。肾功能取决于肾脏产生PG的水平。随着肾脏浓缩能力下降且肾造影结果不尽人意，PGE2排泄量也会减少。盐负荷可导致原发性高血压患者肾脏PG系统功能不全，这表现为在盐负荷早期，与对照值相比，PGE2排泄量的增加要小得多，而PGF2α排泄量则显著增加。在原发性高血压中，肾脏前列腺素对盐负荷的反应不足在一定程度上与肾脏PGE-9-酮还原酶活性改变有关。
