Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1

Abstract Previously, we demonstrated that chronic exposure to low levels of estradiol-17β (E2) increases mean arterial pressure (MAP) in young female Sprague-Dawley (SD) rats, however, the underlying mechanisms are unclear. Since endothelin-1 (ET-1) is implicated in blood pressure (BP) regulation, w...

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Autores principales:	Madhan Subramanian, Sheba M. J. MohanKumar, Priya Balasubramanian, Carrie A. Northcott, Hannah Garver, Gregory D. Fink, P. S. MohanKumar
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5b3d84ddcacc44f88325f3307cfad5de
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spelling	oai:doaj.org-article:5b3d84ddcacc44f88325f3307cfad5de2021-12-02T15:05:39ZChronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-110.1038/s41598-017-00213-92045-2322https://doaj.org/article/5b3d84ddcacc44f88325f3307cfad5de2017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00213-9https://doaj.org/toc/2045-2322Abstract Previously, we demonstrated that chronic exposure to low levels of estradiol-17β (E2) increases mean arterial pressure (MAP) in young female Sprague-Dawley (SD) rats, however, the underlying mechanisms are unclear. Since endothelin-1 (ET-1) is implicated in blood pressure (BP) regulation, we hypothesized that E2’s effects on MAP are mediated through central ET-1. To test this, young female SD rats were either sham implanted or implanted s.c. with slow-release E2 pellets (20 ng/day for 90 days). BP was monitored by telemetry. After 75 days of E2 exposure, ETA antagonist or vehicle was administered i.c.v. After 90 days of E2 exposure, rats were sacrificed, and the paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) were microdissected for gene expression and protein analysis of ET-1 and its receptors. E2 exposure increased MAP after pellet implantation. Gene expression of ET-1 and ETA but not ETB receptors were upregulated in the PVN and RVLM of E2 treated animals. Further, the protein levels of ETA receptor were also increased in the PVN of E2 treated animals. However, i.c.v. infusion of the ETA antagonist did not completely block the increase in blood pressure. Our results suggest that increases in central ET-1 activity could possibly play a role in chronic E2-induced increase in BP but further studies are needed to completely understand the contribution of ET-1 in this phenomenon.Madhan SubramanianSheba M. J. MohanKumarPriya BalasubramanianCarrie A. NorthcottHannah GarverGregory D. FinkP. S. MohanKumarNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Madhan Subramanian Sheba M. J. MohanKumar Priya Balasubramanian Carrie A. Northcott Hannah Garver Gregory D. Fink P. S. MohanKumar Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1
description	Abstract Previously, we demonstrated that chronic exposure to low levels of estradiol-17β (E2) increases mean arterial pressure (MAP) in young female Sprague-Dawley (SD) rats, however, the underlying mechanisms are unclear. Since endothelin-1 (ET-1) is implicated in blood pressure (BP) regulation, we hypothesized that E2’s effects on MAP are mediated through central ET-1. To test this, young female SD rats were either sham implanted or implanted s.c. with slow-release E2 pellets (20 ng/day for 90 days). BP was monitored by telemetry. After 75 days of E2 exposure, ETA antagonist or vehicle was administered i.c.v. After 90 days of E2 exposure, rats were sacrificed, and the paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) were microdissected for gene expression and protein analysis of ET-1 and its receptors. E2 exposure increased MAP after pellet implantation. Gene expression of ET-1 and ETA but not ETB receptors were upregulated in the PVN and RVLM of E2 treated animals. Further, the protein levels of ETA receptor were also increased in the PVN of E2 treated animals. However, i.c.v. infusion of the ETA antagonist did not completely block the increase in blood pressure. Our results suggest that increases in central ET-1 activity could possibly play a role in chronic E2-induced increase in BP but further studies are needed to completely understand the contribution of ET-1 in this phenomenon.
format	article
author	Madhan Subramanian Sheba M. J. MohanKumar Priya Balasubramanian Carrie A. Northcott Hannah Garver Gregory D. Fink P. S. MohanKumar
author_facet	Madhan Subramanian Sheba M. J. MohanKumar Priya Balasubramanian Carrie A. Northcott Hannah Garver Gregory D. Fink P. S. MohanKumar
author_sort	Madhan Subramanian
title	Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1
title_short	Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1
title_full	Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1
title_fullStr	Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1
title_full_unstemmed	Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1
title_sort	chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: a possible role for central endothelin-1
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/5b3d84ddcacc44f88325f3307cfad5de
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Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1

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