Új szempontok a sószenzitív hypertoniák patomechanizmusában

Translated title of the contribution: New aspects of the pathomechanism of salt-sensitive hypertension

Research output: Contribution to journalArticle

Abstract

This article shortly outlines the evolution of hypertonia from risk factors to end-organ damage. The pathogenetic role of salt intake is underlined and in the light of recent clinical and experimental observations, the importance of renal and extrarenal mechanism in the development of salt-sensitive hypertension is analysed. The generally accepted concept that the inefficient renal sodium excretion and the subsequent expansion of the extracellular space is the major factor in blood pressure elevation is challenged. Evidences have been provided that the retained sodium dissociates from the volume of extracellular space and, also from the blood pressure. It has been shown that the negatively charged macromolecules in the subcutaneous interstitium bind sodium ions in osmotically inactive form and store sodium reversibly. The local tissue hypertonicity induces monocytes/macrophages invasion and activation that causes increased expression of tonicity-responsive enhancer binding protein (TonEBP) and the secretion of vascular endothelial growth factor C that result in enhanced lymphangiogenesis. The expanded lymphatic system drains the excess sodium and volume back to the circulation. The reduction of buffer function of this system may contribute to the development or to worsening of hypertension. Similar buffer and barrier functions are attributed to the glycocalyx that covers the luminal surface of vascular endothelium. It is also recognised that the high sodium intake alone is an important pathogenetic factor in end-organ damage independent of hypertension. This may be accounted for by the induction and activation of Th17 cells as well as by the increased production of several pro-inflammatory and pro-fibrotic cytokines.

Original languageHungarian
Pages (from-to)43-49
Number of pages7
JournalOrvosi Hetilap
Volume160
Issue number2
DOIs
Publication statusPublished - Jan 1 2019

Fingerprint

Salts
Sodium
Hypertension
Extracellular Space
Buffers
Lymphangiogenesis
Vascular Endothelial Growth Factor C
NFATC Transcription Factors
Blood Pressure
Glycocalyx
Th17 Cells
Lymphatic System
Macrophage Activation
Vascular Endothelium
Monocytes
Ions
Cytokines
Kidney

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Új szempontok a sószenzitív hypertoniák patomechanizmusában. / Sulyok, E.

In: Orvosi Hetilap, Vol. 160, No. 2, 01.01.2019, p. 43-49.

Research output: Contribution to journalArticle

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