Hypertension in Metabolic Syndrome: Vascular Pathophysiology

Metabolic syndrome is a cluster of metabolic and cardiovascular symptoms: insulin resistance (IR), obesity, dyslipemia. Hypertension and vascular disorders are central to this syndrome. After a brief historical review, we discuss the role of sympathetic tone. Subsequently, we examine the link betwee...

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Main Authors: Yolanda Mendizábal, Silvia Llorens, Eduardo Nava
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:International Journal of Hypertension
Online Access:http://dx.doi.org/10.1155/2013/230868
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author Yolanda Mendizábal
Silvia Llorens
Eduardo Nava
author_facet Yolanda Mendizábal
Silvia Llorens
Eduardo Nava
author_sort Yolanda Mendizábal
collection DOAJ
description Metabolic syndrome is a cluster of metabolic and cardiovascular symptoms: insulin resistance (IR), obesity, dyslipemia. Hypertension and vascular disorders are central to this syndrome. After a brief historical review, we discuss the role of sympathetic tone. Subsequently, we examine the link between endothelial dysfunction and IR. NO is involved in the insulin-elicited capillary vasodilatation. The insulin-signaling pathways causing NO release are different to the classical. There is a vasodilatory pathway with activation of NO synthase through Akt, and a vasoconstrictor pathway that involves the release of endothelin-1 via MAPK. IR is associated with an imbalance between both pathways in favour of the vasoconstrictor one. We also consider the link between hypertension and IR: the insulin hypothesis of hypertension. Next we discuss the importance of perivascular adipose tissue and the role of adipokines that possess vasoactive properties. Finally, animal models used in the study of vascular function of metabolic syndrome are reviewed. In particular, the Zucker fatty rat and the spontaneously hypertensive obese rat (SHROB). This one suffers macro- and microvascular malfunction due to a failure in the NO system and an abnormally high release of vasoconstrictor prostaglandins, all this alleviated with glitazones used for metabolic syndrome therapy.
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spelling doaj-art-344e9638971f46c0a4940f011aaffc9b2025-02-03T01:01:04ZengWileyInternational Journal of Hypertension2090-03842090-03922013-01-01201310.1155/2013/230868230868Hypertension in Metabolic Syndrome: Vascular PathophysiologyYolanda Mendizábal0Silvia Llorens1Eduardo Nava2Department of Medical Sciences, University of Castilla-La Mancha, School of Medicine and Regional Centre for Biomedical Research (CRIB), 02006 Albacete, SpainDepartment of Medical Sciences, University of Castilla-La Mancha, School of Medicine and Regional Centre for Biomedical Research (CRIB), 02006 Albacete, SpainDepartment of Medical Sciences, University of Castilla-La Mancha, School of Medicine and Regional Centre for Biomedical Research (CRIB), 02006 Albacete, SpainMetabolic syndrome is a cluster of metabolic and cardiovascular symptoms: insulin resistance (IR), obesity, dyslipemia. Hypertension and vascular disorders are central to this syndrome. After a brief historical review, we discuss the role of sympathetic tone. Subsequently, we examine the link between endothelial dysfunction and IR. NO is involved in the insulin-elicited capillary vasodilatation. The insulin-signaling pathways causing NO release are different to the classical. There is a vasodilatory pathway with activation of NO synthase through Akt, and a vasoconstrictor pathway that involves the release of endothelin-1 via MAPK. IR is associated with an imbalance between both pathways in favour of the vasoconstrictor one. We also consider the link between hypertension and IR: the insulin hypothesis of hypertension. Next we discuss the importance of perivascular adipose tissue and the role of adipokines that possess vasoactive properties. Finally, animal models used in the study of vascular function of metabolic syndrome are reviewed. In particular, the Zucker fatty rat and the spontaneously hypertensive obese rat (SHROB). This one suffers macro- and microvascular malfunction due to a failure in the NO system and an abnormally high release of vasoconstrictor prostaglandins, all this alleviated with glitazones used for metabolic syndrome therapy.http://dx.doi.org/10.1155/2013/230868
spellingShingle Yolanda Mendizábal
Silvia Llorens
Eduardo Nava
Hypertension in Metabolic Syndrome: Vascular Pathophysiology
International Journal of Hypertension
title Hypertension in Metabolic Syndrome: Vascular Pathophysiology
title_full Hypertension in Metabolic Syndrome: Vascular Pathophysiology
title_fullStr Hypertension in Metabolic Syndrome: Vascular Pathophysiology
title_full_unstemmed Hypertension in Metabolic Syndrome: Vascular Pathophysiology
title_short Hypertension in Metabolic Syndrome: Vascular Pathophysiology
title_sort hypertension in metabolic syndrome vascular pathophysiology
url http://dx.doi.org/10.1155/2013/230868
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AT silviallorens hypertensioninmetabolicsyndromevascularpathophysiology
AT eduardonava hypertensioninmetabolicsyndromevascularpathophysiology