Kutyrina I M, Rogov V A, Lifshits N L, Tatsievskiĭ V A
Ter Arkh. 1987;59(11):75-80.
The activity of the renin-angiotensin-aldosterone system (RAAS), excretion of renal prostaglandins, renal hemodynamics, water-electrolyte balance were studied in 110 patients with chronic nephritis with arterial hypertension: 47 with hypertonic nephritis and 63 patients at the stage of renal insufficiency. Some investigations, the results of data processing, an analysis of the results of cross-group comparative studies, and the use of captopril (a drug that inhibits the activity of angiotensin-converting enzymes) confirmed the RAAS involvement in the pathogenesis of arterial hypertension in nephritides. Pathophysiological features of arterial hypertension in nephritides are the following: disturbances of physiological interrelationships between renin plasma activity and the state of water-electrolyte balance; hyperaldosteronism and depression of renal prostaglandin synthesis revealed both in unchanged and lowered renal function. The peculiarity of arterial hypertension at the stage of marked renal insufficiency is invariability of renin production resulting from structural reserves of the renal juxtaglomerular apparatus.
对110例患有动脉高血压的慢性肾炎患者进行了肾素-血管紧张素-醛固酮系统(RAAS)活性、肾前列腺素排泄、肾血流动力学及水电解质平衡的研究:其中47例为高血压性肾炎患者,63例处于肾功能不全阶段。一些研究、数据处理结果、组间对比研究结果分析以及卡托普利(一种抑制血管紧张素转换酶活性的药物)的使用证实,RAAS参与了肾炎性动脉高血压的发病机制。肾炎性动脉高血压的病理生理特征如下:肾素血浆活性与水电解质平衡状态之间生理关系紊乱;醛固酮增多症以及无论肾功能正常或降低时均出现的肾前列腺素合成受抑制。明显肾功能不全阶段动脉高血压的特点是,由于肾球旁器的结构储备,肾素产生不变。