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      Estrogen therapy may counterbalance eutrophic remodeling of coronary arteries and increase bradykinin relaxation in a rat model of menopausal hypertension

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          Abstract

          Objective:

          Hypertension causes adverse remodeling and vasomotor alterations in coronaries. Hormones such as estrogen may help counterbalance some of these effects. The aim of this study was to analyze the effects of ovariectomy and estrogen therapy in a rat model of menopausal hypertension induced by angiotensin II (AII).

          Methods:

          We investigated diameter, tone, and mechanics of intramural coronaries taken from ovariectomized female rats (n = 11) that received chronic AII treatment to induce hypertension, and compared the results with those found in female rats that were also given estrogen therapy (n = 11). The “hypertensive control” group (n = 11) underwent an abdominal sham operation, and received AII. After 4 weeks of AII treatment, side branches of left anterior descendent coronary (approximately 200 μm in diameter) were isolated, cannulated with plastic microcannulas at both ends, and studied in vitro in a vessel chamber. The inner and outer diameter of the arteries were measured by microangiometry, and spontenuous tone, wall thickness, wall cross-sectional area, tangential stress, incremental distensibility, circumferential incremental elastic modulus, thromboxane agonist-induced tone, and bradykinin-induced dilation were calculated.

          Results:

          In hypertension, intramural small coronaries show inward eutrophic remodeling after ovariectomy comparing with hypertensive controls. Estrogen therapy had an opposite effect on vessel diameter. Hormone therapy led to an increase in spontaneous tone, allowing for greater dilatative capacity.

          Conclusions:

          Estrogen may therefore be considered to counterbalance some of the adverse changes seen in the wall of intramural coronaries in the early stages of chronic hypertension.

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          Most cited references18

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          Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan.

          Structural and functional alterations of the vasculature may contribute to complications of hypertension. Because angiotensin II may be pivotal in some of these vascular abnormalities, we tested the hypothesis that the angiotensin type 1 (AT(1)) receptor antagonist losartan, in contrast to the beta-blocker atenolol, would correct resistance artery abnormalities in patients with essential hypertension. Nineteen untreated patients with mild essential hypertension (47+/-2 years, range 30 to 65 years; 57% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for 1 year. Nine age/sex-matched normotensive subjects were also studied. Both treatments reduced blood pressure to a comparable degree (losartan, from 149+/-4.1/101+/-1.6 to 128+/-3.6/86+/-2.2 mm Hg, P<0.01; atenolol, from 150+/-4.0/99+/-1.2 to 130+/-3.2/84+/-1.4 mm Hg, P<0.01). Resistance arteries (luminal diameter 150 to 350 microm) dissected from gluteal subcutaneous biopsies were studied on a pressurized myograph. After 1 year of treatment, the ratio of the media width to lumen diameter of arteries from losartan-treated patients was significantly reduced (from 8.4+/-0.4% to 6.7+/-0.3%, P<0.01). Arteries from atenolol-treated patients exhibited no significant change (from 8. 3+/-0.3% to 8.8+/-0.5% after treatment). Endothelium-dependent relaxation (acetylcholine-induced) was normalized by losartan (from 82.1+/-4.9% to 94.7+/-1.1%, P<0.01) but not by atenolol (from 80. 4+/-2.7% to 81.7+/-4.6%). Endothelium-independent relaxation (by sodium nitroprusside) was unchanged after treatment. The AT(1) antagonist losartan corrected the altered structure and endothelial dysfunction of resistance arteries from patients with essential hypertension, whereas the beta-blocker atenolol had no effect.
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            Small artery remodeling and significance in the development of hypertension.

            The structure of the resistance vessels is altered (remodeled) in individuals with high blood pressure (essential hypertension). The structure is dependent not only on blood pressure but also on blood flow and hormonal environment. Vascular biology is providing increased knowledge of the mechanisms involved and thus contributing to our understanding of the pathophysiology of the disease.
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              Vascular remodelling of resistance vessels: can we define this?

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                Author and article information

                Journal
                Menopause
                Menopause
                MENOP
                Menopause (New York, N.y.)
                Lippincott-Raven Publishers
                1072-3714
                1530-0374
                July 2016
                07 July 2016
                : 23
                : 7
                : 778-783
                Affiliations
                [1 ]Institute of Human Physiology and Clinical Experimental Research
                [2 ]Department of Orthopedics
                [3 ]Department of Physiology
                [4 ]2nd Department of Internal Medicine—Department Section of Geriatrics
                [5 ]2nd Department of Obstetrics and Gynecology, Faculty of Medicine, Semmelweis University, Budapest, Hungary
                [6 ]Department of Obstetrics and Gynecology, Meir Medical Center, Kfar Saba, affiliated with Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
                Author notes
                Address correspondence to: Judit R. Hetthéssy, MD, Department of Orthopaedics, Semmelweis University, Karolina út 27, 1113 Budapest, Hungary. E-mail: drhjr612@ 123456gmail.com
                Article
                10.1097/GME.0000000000000654
                4927223
                27187011
                505e8717-fbaf-4860-b351-c6da43ecede4
                © 2016 by The North American Menopause Society

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/4.0

                History
                : 25 October 2015
                : 18 February 2015
                : 18 February 2015
                Categories
                Original Articles
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                coronary,contractility,ovariectomy,estrogen therapy,angiotensin ii,menopausal hypertension

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