Abstract
Arterial hypertension (AH) in patients with chronic renal pathology is a result of a damage and impaired function of the kidneys involved in the maintenance of the water-salt and circulatory homeostasis. The progressing damage of the renal tissue, in addition to activation of the circulating renin-angiotensin- aldosterone system (RAAS) characteristic of the hyper-renin form of nephrogenic AH, brings on reflectory stimulation of the central structures sympathetic system, which lead to growing sympathetic influence on the cardiovascular system and kidneys. A characteristic feature of the neuro-humoral status of patients with normo- , and especially with hyporenin forms of nephrogenic AH is an elevated activity of endothelin system of the vessels. Formed in the kidneys disbalance of neurohumoral systems is accompanied by excessive reabsorption of sodium, which not only suppresses the mechanism of pressor natriuresis contributing to stabilization of AH at a higher level, but causes its delay in organism, providing for the development of volume-dependent and salt-sensitive AH.
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