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.
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