Evidence about the crucial role of the kidney in the development and maintenance of the „essential“ hypertension (i.e. hypertension which is accompanied with the absence of any pathological change in any of body organs) and in the regulation of „normal“ blood pressure level (BP) has been accumulated. Blood pressure is expressed as a product of cardiac output (CO) and total peripheral resistance (TPR). TPR almost entirely depends on the volume of the extracellular fluid (ECFV): With increasing volume BP rises and vice versa. ECFV – due to intensive maintenance of the osmolality – almost entirely depends on the total amount of sodium in the organism. This amount is not determined by the intake of salt, which is in every civilised population always higher than necessary. Sodium balance is therefore critically determined by the output of sodium, which is carried out almost entirely by the kidney. The output depends on the quantity of the glomerular filtration and on the tubular reabsorption. Under normal circumstances, the increased sodium intake is accompanied by an increased excretion via the mechanism called „pressure natriuresis“. It is based on the prompt increase of sodium excretion after an increase of BP, resulting from the increased sodium intake. Mechanism of such elevated excretion is not clear; lot of evidence has been accumulated for the existence of a humoral principle produced within the kidney. Such assumption is supported by experiments in which a kidney is transplanted from a hypertonic donor to a normotensive recipient: hypertension in the recipient develops. Similarly, k idney grafting from a normoten- sive animal corrects the hypertension in an originally hypertensive recipient. Important role of the renin-angio- tensin (RAS) and nitric oxide (NO) systems is often stressed in this context. If kidney is unable to excrete the ingested amount of sodium at the normal BP, blood pressure must rise and the shift of the pressure-natriuresis curve to the right is the necessary consequence. If these conditions are long lasting, hypertension develops soon and becomes „fixed“ by rebuilding the resistance arteries architecture.

        Key words: hypertension, extracellular fluid volume, pressure-natriuresis, nitric oxide, renin-angiotensin