Inositol 1,4,5-Trisphosphate Receptors in Hypertension

<p dir="ltr">Chronic hypertension remains a major cause of global mortality and morbidity. It is a complex disease that is the clinical manifestation of multiple genetic, environmental, nutritional, hormonal, and aging-related disorders. Evidence supports a role for vascular aging in...

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Main Author: Ali H. Eid (5461829) (author)
Other Authors: Ahmed F. El-Yazbi (10180589) (author), Fouad Zouein (18091168) (author), Abdelilah Arredouani (10914455) (author), Allal Ouhtit (526) (author), Md M. Rahman (14152977) (author), Hatem Zayed (835448) (author), Gianfranco Pintus (91638) (author), Haissam Abou-Saleh (497840) (author)
Published: 2018
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author Ali H. Eid (5461829)
author2 Ahmed F. El-Yazbi (10180589)
Fouad Zouein (18091168)
Abdelilah Arredouani (10914455)
Allal Ouhtit (526)
Md M. Rahman (14152977)
Hatem Zayed (835448)
Gianfranco Pintus (91638)
Haissam Abou-Saleh (497840)
author2_role author
author
author
author
author
author
author
author
author_facet Ali H. Eid (5461829)
Ahmed F. El-Yazbi (10180589)
Fouad Zouein (18091168)
Abdelilah Arredouani (10914455)
Allal Ouhtit (526)
Md M. Rahman (14152977)
Hatem Zayed (835448)
Gianfranco Pintus (91638)
Haissam Abou-Saleh (497840)
author_role author
dc.creator.none.fl_str_mv Ali H. Eid (5461829)
Ahmed F. El-Yazbi (10180589)
Fouad Zouein (18091168)
Abdelilah Arredouani (10914455)
Allal Ouhtit (526)
Md M. Rahman (14152977)
Hatem Zayed (835448)
Gianfranco Pintus (91638)
Haissam Abou-Saleh (497840)
dc.date.none.fl_str_mv 2018-07-26T03:00:00Z
dc.identifier.none.fl_str_mv 10.3389/fphys.2018.01018
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/Inositol_1_4_5-Trisphosphate_Receptors_in_Hypertension/25331323
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biomedical and clinical sciences
Medical physiology
aging
hypertension
Ca2+
IP3R
VSMC
dc.title.none.fl_str_mv Inositol 1,4,5-Trisphosphate Receptors in Hypertension
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p dir="ltr">Chronic hypertension remains a major cause of global mortality and morbidity. It is a complex disease that is the clinical manifestation of multiple genetic, environmental, nutritional, hormonal, and aging-related disorders. Evidence supports a role for vascular aging in the development of hypertension involving an impairment in endothelial function together with an alteration in vascular smooth muscle cells (VSMCs) calcium homeostasis leading to increased myogenic tone. Changes in free intracellular calcium levels ([Ca<sup>2+</sup>]<sub><em>i</em></sub>) are mediated either by the influx of Ca<sup>2+</sup> from the extracellular space or release of Ca<sup>2+</sup> from intracellular stores, mainly the sarcoplasmic reticulum (SR). The influx of extracellular Ca<sup>2+</sup> occurs primarily through voltage-gated Ca<sup>2+</sup> channels (VGCCs), store-operated Ca<sup>2+</sup> channels (SOC), and Ca<sup>2+</sup> release-activated channels (CRAC), whereas SR-Ca<sup>2+</sup> release occurs through inositol trisphosphate receptor (IP<sub>3</sub>R) and ryanodine receptors (RyRs). IP<sub>3</sub>R-mediated SR-Ca<sup>2+</sup> release, in the form of Ca<sup>2+</sup> waves, not only contributes to VSMC contraction and regulates VGCC function but is also intimately involved in structural remodeling of resistance arteries in hypertension. This involves a phenotypic switch of VSMCs as well as an alteration of cytoplasmic Ca<sup>2+</sup> signaling machinery, a phenomena tightly related to the aging process. Several lines of evidence implicate changes in expression/function levels of IP<sub>3</sub>R isoforms in the development of hypertension, VSMC phenotypic switch, and vascular aging. The present review discusses the current knowledge of these mechanisms in an integrative approach and further suggests potential new targets for hypertension management and treatment.</p><h2>Other Information</h2><p dir="ltr">Published in: Frontiers in Physiology<br>License: <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank">https://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.3389/fphys.2018.01018" target="_blank">https://dx.doi.org/10.3389/fphys.2018.01018</a></p>
eu_rights_str_mv openAccess
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identifier_str_mv 10.3389/fphys.2018.01018
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spelling Inositol 1,4,5-Trisphosphate Receptors in HypertensionAli H. Eid (5461829)Ahmed F. El-Yazbi (10180589)Fouad Zouein (18091168)Abdelilah Arredouani (10914455)Allal Ouhtit (526)Md M. Rahman (14152977)Hatem Zayed (835448)Gianfranco Pintus (91638)Haissam Abou-Saleh (497840)Biomedical and clinical sciencesMedical physiologyaginghypertensionCa2+IP3RVSMC<p dir="ltr">Chronic hypertension remains a major cause of global mortality and morbidity. It is a complex disease that is the clinical manifestation of multiple genetic, environmental, nutritional, hormonal, and aging-related disorders. Evidence supports a role for vascular aging in the development of hypertension involving an impairment in endothelial function together with an alteration in vascular smooth muscle cells (VSMCs) calcium homeostasis leading to increased myogenic tone. Changes in free intracellular calcium levels ([Ca<sup>2+</sup>]<sub><em>i</em></sub>) are mediated either by the influx of Ca<sup>2+</sup> from the extracellular space or release of Ca<sup>2+</sup> from intracellular stores, mainly the sarcoplasmic reticulum (SR). The influx of extracellular Ca<sup>2+</sup> occurs primarily through voltage-gated Ca<sup>2+</sup> channels (VGCCs), store-operated Ca<sup>2+</sup> channels (SOC), and Ca<sup>2+</sup> release-activated channels (CRAC), whereas SR-Ca<sup>2+</sup> release occurs through inositol trisphosphate receptor (IP<sub>3</sub>R) and ryanodine receptors (RyRs). IP<sub>3</sub>R-mediated SR-Ca<sup>2+</sup> release, in the form of Ca<sup>2+</sup> waves, not only contributes to VSMC contraction and regulates VGCC function but is also intimately involved in structural remodeling of resistance arteries in hypertension. This involves a phenotypic switch of VSMCs as well as an alteration of cytoplasmic Ca<sup>2+</sup> signaling machinery, a phenomena tightly related to the aging process. Several lines of evidence implicate changes in expression/function levels of IP<sub>3</sub>R isoforms in the development of hypertension, VSMC phenotypic switch, and vascular aging. The present review discusses the current knowledge of these mechanisms in an integrative approach and further suggests potential new targets for hypertension management and treatment.</p><h2>Other Information</h2><p dir="ltr">Published in: Frontiers in Physiology<br>License: <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank">https://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.3389/fphys.2018.01018" target="_blank">https://dx.doi.org/10.3389/fphys.2018.01018</a></p>2018-07-26T03:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.3389/fphys.2018.01018https://figshare.com/articles/journal_contribution/Inositol_1_4_5-Trisphosphate_Receptors_in_Hypertension/25331323CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/253313232018-07-26T03:00:00Z
spellingShingle Inositol 1,4,5-Trisphosphate Receptors in Hypertension
Ali H. Eid (5461829)
Biomedical and clinical sciences
Medical physiology
aging
hypertension
Ca2+
IP3R
VSMC
status_str publishedVersion
title Inositol 1,4,5-Trisphosphate Receptors in Hypertension
title_full Inositol 1,4,5-Trisphosphate Receptors in Hypertension
title_fullStr Inositol 1,4,5-Trisphosphate Receptors in Hypertension
title_full_unstemmed Inositol 1,4,5-Trisphosphate Receptors in Hypertension
title_short Inositol 1,4,5-Trisphosphate Receptors in Hypertension
title_sort Inositol 1,4,5-Trisphosphate Receptors in Hypertension
topic Biomedical and clinical sciences
Medical physiology
aging
hypertension
Ca2+
IP3R
VSMC