The history of research on kidney role in arterial hypertension begins in 1892 when Brown-Sequard suggested internal secretion of kidneys that causes hypertension.
Since then we observe dynamic development of laboratory assessments that allowed to discover and understand activity of renin–angiotensin–aldosterone system. This system works as a feedback mechanism and plays the key role in regulation of blood pressure (BP) by angiotensin secretion and sodium-volume status by aldosterone release. Laragh and Alderman assume that cardiac output CO) is determined by sodium-volume factor while vasoconstriction (total peripheral resistance — TPR) results from plasma renin-angiotensin concentration. (BP) = CO × TPR. Using plasma renin activity (PRA) value it is possible to divide all hypertensive patients into two basic subtypes. PRA > 0.65 ng/ml/h is connected with the renin–angiotensin mediated vasoconstrictor hypertension („R” hypertension) and PRA < 0.65 ng/ml/h is connected with sodium-volume mediated hypertension („V” hypertension). „R” hypertension is diagnosed in 60–70% of hypertensive patients and „V” hypertension in 30–40%. Different mechanisms of antihypertensive drugs action determine usefulness of them in a given type of hypertension. ACEIs, ARBs and beta-blockers represent „R” drugs that block plasma renin system. Diuretics, calcium channel blockers and alpha-blockers belong to „V” drugs that reduce sodium-volume component. Laragh and Alderman, two eminent scientists and practitioners, show us that giving proper „R” or „V” drug it is possible to achieve therapeutic goals with just a monotherapy. In this article we try to analyse if such simple pathophysiological hypothesis of arterial hypertension should be still implemented in everyday clinical practice.