Favourable results with the use of inhibitors of the angiotension I-converting enzyme in the therapy not only of high-renin but also normo-renin and low-renin hypertension revived interest in research in the area of the renin-angiotensin (RAS) system. The use of classical radioimmunological, radiohistochemical receptor studies as well as of recent methods of molecular biology and pathology revealed that for the regulation of blood pressure and the extracellular volume and pathogenesis of hypertension not only RAS components in systemic blood are important but also local tissue RAS with an autocrine and paracrine action at the site of its origin. Cerebral RAS participates in the central cardiovascular regulation, in the control of the salt and water intake, the secretion of antidiuretic hormone and ACTH. In the cardiovascular apparatus RAS is responsible not only for vasoconstriction but it acts also as a growth factor promoting the development of cardiac and vascular hypertrophy. In the kidneys RAS decides on the blood flow, its distribution, glomerular filtration. Its excessive stimulation may contribute in arterial hypertension, diabetic nephropathy and in residual nephrons during chronic renal failure, to the change from functional hyperfiltration to irreversible structural damage of the nephron. Inhibitors of the converting enzyme not only reduce the peripheral vascular resistance in arterial hypertension but influence also the tissue production of angiotensin II and thus the regression of cardiovascular hypertrophy and progression of renal damage.