Contribution of neurohumoral dysfunction and overweight to the course of essential hypertension

Aim. To determine the role of neurohumoral dysfunction and overweight in a clinical course of arterial hypertension (AH). Material and methods. 200 participants of the study aged 30-60 years with AH degree I-II with low, moderate and high overall cardiovascular risk and mean disease duration 11.1 ±...

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Main Author: S S Bunova
Format: Article
Language:Russian
Published: "Consilium Medicum" Publishing house 2009-05-01
Series:Терапевтический архив
Subjects:
Online Access:https://ter-arkhiv.ru/0040-3660/article/view/30368
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spelling doaj-fbef6b6e4c52429e9e56ec56535c9b6b2020-11-25T03:02:56Zrus"Consilium Medicum" Publishing houseТерапевтический архив0040-36602309-53422009-05-01815717427395Contribution of neurohumoral dysfunction and overweight to the course of essential hypertensionS S BunovaS S BunovaAim. To determine the role of neurohumoral dysfunction and overweight in a clinical course of arterial hypertension (AH). Material and methods. 200 participants of the study aged 30-60 years with AH degree I-II with low, moderate and high overall cardiovascular risk and mean disease duration 11.1 ± 9.5 years were examined for body mass index, levels of leptin, soluble leptin receptor, insulin, serotonin and adrenoreactivity. Results. Neurohumoral dysfunction correlated with body mass index. It manifested with elevation of insulin and leptin levels, sympathetic hyperactivity and a decrease of serotonin. Conclusion. One of the mechanisms forming and sustaining AH in patients with overweight is leptin-dependent sympathetic hyperactivity while serotonin system activation is more important for patients with normal body weight. Hypertensive patients with obesity demonstrate insulin-dependent hyperleptinemia.https://ter-arkhiv.ru/0040-3660/article/view/30368arterial hypertensionleptinserotoninsympathetic hyperactivity
collection DOAJ
language Russian
format Article
sources DOAJ
author S S Bunova
S S Bunova
spellingShingle S S Bunova
S S Bunova
Contribution of neurohumoral dysfunction and overweight to the course of essential hypertension
Терапевтический архив
arterial hypertension
leptin
serotonin
sympathetic hyperactivity
author_facet S S Bunova
S S Bunova
author_sort S S Bunova
title Contribution of neurohumoral dysfunction and overweight to the course of essential hypertension
title_short Contribution of neurohumoral dysfunction and overweight to the course of essential hypertension
title_full Contribution of neurohumoral dysfunction and overweight to the course of essential hypertension
title_fullStr Contribution of neurohumoral dysfunction and overweight to the course of essential hypertension
title_full_unstemmed Contribution of neurohumoral dysfunction and overweight to the course of essential hypertension
title_sort contribution of neurohumoral dysfunction and overweight to the course of essential hypertension
publisher "Consilium Medicum" Publishing house
series Терапевтический архив
issn 0040-3660
2309-5342
publishDate 2009-05-01
description Aim. To determine the role of neurohumoral dysfunction and overweight in a clinical course of arterial hypertension (AH). Material and methods. 200 participants of the study aged 30-60 years with AH degree I-II with low, moderate and high overall cardiovascular risk and mean disease duration 11.1 ± 9.5 years were examined for body mass index, levels of leptin, soluble leptin receptor, insulin, serotonin and adrenoreactivity. Results. Neurohumoral dysfunction correlated with body mass index. It manifested with elevation of insulin and leptin levels, sympathetic hyperactivity and a decrease of serotonin. Conclusion. One of the mechanisms forming and sustaining AH in patients with overweight is leptin-dependent sympathetic hyperactivity while serotonin system activation is more important for patients with normal body weight. Hypertensive patients with obesity demonstrate insulin-dependent hyperleptinemia.
topic arterial hypertension
leptin
serotonin
sympathetic hyperactivity
url https://ter-arkhiv.ru/0040-3660/article/view/30368
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