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Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension

One of the major pathophysiological features of primary hypertension is an inappropriate activation of the sympathetic nervous system, which is mediated by excessive synthesis and secretion of catecholamine into the blood. Tyrosine hydroxylase (TH), a rate-limiting enzyme in the synthesis of catecho...

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Autores principales: Lee, Yu Ho, Kim, Yang Gyun, Moon, Ju-Young, Kim, Jin Sug, Jeong, Kyung-Hwan, Lee, Tae Won, Ihm, Chun-Gyoo, Lee, Sang Ho
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Electrolyte Metabolism 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5337429/
https://www.ncbi.nlm.nih.gov/pubmed/28275384
http://dx.doi.org/10.5049/EBP.2016.14.2.21
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author Lee, Yu Ho
Kim, Yang Gyun
Moon, Ju-Young
Kim, Jin Sug
Jeong, Kyung-Hwan
Lee, Tae Won
Ihm, Chun-Gyoo
Lee, Sang Ho
author_facet Lee, Yu Ho
Kim, Yang Gyun
Moon, Ju-Young
Kim, Jin Sug
Jeong, Kyung-Hwan
Lee, Tae Won
Ihm, Chun-Gyoo
Lee, Sang Ho
author_sort Lee, Yu Ho
collection PubMed
description One of the major pathophysiological features of primary hypertension is an inappropriate activation of the sympathetic nervous system, which is mediated by excessive synthesis and secretion of catecholamine into the blood. Tyrosine hydroxylase (TH), a rate-limiting enzyme in the synthesis of catecholamine, has been highlighted because genetic variations of TH could alter the activity of the sympathetic nervous system activity and subsequently contribute to the pathogenesis of hypertension. Here, we discuss the role of TH as a regulator of sympathetic activity and review several studies that investigated the relationship between genetic variations of TH and hypertension.
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spelling pubmed-53374292017-03-08 Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension Lee, Yu Ho Kim, Yang Gyun Moon, Ju-Young Kim, Jin Sug Jeong, Kyung-Hwan Lee, Tae Won Ihm, Chun-Gyoo Lee, Sang Ho Electrolyte Blood Press Review One of the major pathophysiological features of primary hypertension is an inappropriate activation of the sympathetic nervous system, which is mediated by excessive synthesis and secretion of catecholamine into the blood. Tyrosine hydroxylase (TH), a rate-limiting enzyme in the synthesis of catecholamine, has been highlighted because genetic variations of TH could alter the activity of the sympathetic nervous system activity and subsequently contribute to the pathogenesis of hypertension. Here, we discuss the role of TH as a regulator of sympathetic activity and review several studies that investigated the relationship between genetic variations of TH and hypertension. The Korean Society of Electrolyte Metabolism 2016-12 2016-12-31 /pmc/articles/PMC5337429/ /pubmed/28275384 http://dx.doi.org/10.5049/EBP.2016.14.2.21 Text en Copyright © 2016 The Korean Society of Electrolyte Metabolism http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Lee, Yu Ho
Kim, Yang Gyun
Moon, Ju-Young
Kim, Jin Sug
Jeong, Kyung-Hwan
Lee, Tae Won
Ihm, Chun-Gyoo
Lee, Sang Ho
Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension
title Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension
title_full Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension
title_fullStr Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension
title_full_unstemmed Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension
title_short Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension
title_sort genetic variations of tyrosine hydroxylase in the pathogenesis of hypertension
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5337429/
https://www.ncbi.nlm.nih.gov/pubmed/28275384
http://dx.doi.org/10.5049/EBP.2016.14.2.21
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