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Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin–angiotensin system

Hypertension in postmenopausal women is less well controlled than in age‐matched men. The aging female SHR is a model of postmenopausal hypertension that is mediated in part by activation of the renin–angiotensin system (RAS) and by the renal sympathetic nervous system. In this study, the hypothesis...

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Autores principales: Maranon, Rodrigo O., Reckelhoff, Jane F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760383/
https://www.ncbi.nlm.nih.gov/pubmed/26811052
http://dx.doi.org/10.14814/phy2.12669
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author Maranon, Rodrigo O.
Reckelhoff, Jane F.
author_facet Maranon, Rodrigo O.
Reckelhoff, Jane F.
author_sort Maranon, Rodrigo O.
collection PubMed
description Hypertension in postmenopausal women is less well controlled than in age‐matched men. The aging female SHR is a model of postmenopausal hypertension that is mediated in part by activation of the renin–angiotensin system (RAS) and by the renal sympathetic nervous system. In this study, the hypothesis was tested that renal denervation would lower the blood pressure in old female SHR and would attenuate the antihypertensive effects of AT1 receptor antagonism. Retired breeder female SHR were subjected to right uninephrectomy (UNX) and left renal denervation (RD) or UNX and sham, and 2 weeks later, baseline mean arterial pressure (MAP; radiotelemetry) was measured for 4 days, and then rats were treated with angiotensin (AT1) receptor antagonist, losartan (40 mg/kg/day po) for 6 days. Renal denervation reduced MAP in old females compared to sham (172 ± 6 vs. 193 ± 6 mm Hg; P < 0.05). Losartan reduced MAP in both sham and RD rats similarly (numerically and by percentage) (142 ± 10 vs. 161 ± 6 mm Hg; P < 0.05 vs. RD, P < 0.05 vs. baseline). However, female SHR rats remained significantly hypertensive despite both pharmacological intervention and RD. The data suggest that both the renal sympathetic nervous system and the RAS have independent effects to control the blood pressure in old female SHR. Since the denervated rats treated with losartan remained hypertensive, the data also suggest that other mechanisms than the RAS and renal sympathetic nervous system contribute to the hypertension in old female SHR. The data also suggest that multiple mechanisms may mediate the elevated blood pressure in postmenopausal women.
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spelling pubmed-47603832016-02-22 Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin–angiotensin system Maranon, Rodrigo O. Reckelhoff, Jane F. Physiol Rep Original Research Hypertension in postmenopausal women is less well controlled than in age‐matched men. The aging female SHR is a model of postmenopausal hypertension that is mediated in part by activation of the renin–angiotensin system (RAS) and by the renal sympathetic nervous system. In this study, the hypothesis was tested that renal denervation would lower the blood pressure in old female SHR and would attenuate the antihypertensive effects of AT1 receptor antagonism. Retired breeder female SHR were subjected to right uninephrectomy (UNX) and left renal denervation (RD) or UNX and sham, and 2 weeks later, baseline mean arterial pressure (MAP; radiotelemetry) was measured for 4 days, and then rats were treated with angiotensin (AT1) receptor antagonist, losartan (40 mg/kg/day po) for 6 days. Renal denervation reduced MAP in old females compared to sham (172 ± 6 vs. 193 ± 6 mm Hg; P < 0.05). Losartan reduced MAP in both sham and RD rats similarly (numerically and by percentage) (142 ± 10 vs. 161 ± 6 mm Hg; P < 0.05 vs. RD, P < 0.05 vs. baseline). However, female SHR rats remained significantly hypertensive despite both pharmacological intervention and RD. The data suggest that both the renal sympathetic nervous system and the RAS have independent effects to control the blood pressure in old female SHR. Since the denervated rats treated with losartan remained hypertensive, the data also suggest that other mechanisms than the RAS and renal sympathetic nervous system contribute to the hypertension in old female SHR. The data also suggest that multiple mechanisms may mediate the elevated blood pressure in postmenopausal women. John Wiley and Sons Inc. 2016-01-26 /pmc/articles/PMC4760383/ /pubmed/26811052 http://dx.doi.org/10.14814/phy2.12669 Text en © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Maranon, Rodrigo O.
Reckelhoff, Jane F.
Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin–angiotensin system
title Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin–angiotensin system
title_full Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin–angiotensin system
title_fullStr Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin–angiotensin system
title_full_unstemmed Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin–angiotensin system
title_short Mechanisms responsible for postmenopausal hypertension in a rat model: Roles of the renal sympathetic nervous system and the renin–angiotensin system
title_sort mechanisms responsible for postmenopausal hypertension in a rat model: roles of the renal sympathetic nervous system and the renin–angiotensin system
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760383/
https://www.ncbi.nlm.nih.gov/pubmed/26811052
http://dx.doi.org/10.14814/phy2.12669
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