Authors:
M. Matrai Semmelweis University and Department Geriatrics, National Institute of Psychiatry & Neurology Institute of Human Physiology and Clinical Experimental Research Budapest Hungary

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B. Szekacs Semmelweis University and Department Geriatrics, National Institute of Psychiatry & Neurology 2nd Department of Internal Medicine — Department Section of Geriatrics, Faculty of Medicine Budapest Hungary

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M. Mericli Semmelweis University and Department Geriatrics, National Institute of Psychiatry & Neurology 2nd Department of Obstetrics and Gynecology Budapest Hungary

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G. Nadasy Semmelweis University and Department Geriatrics, National Institute of Psychiatry & Neurology Institute of Human Physiology and Clinical Experimental Research Budapest Hungary

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M. Szekeres Semmelweis University and Department Geriatrics, National Institute of Psychiatry & Neurology Institute of Human Physiology and Clinical Experimental Research Budapest Hungary

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F. Banhidy Semmelweis University and Department Geriatrics, National Institute of Psychiatry & Neurology 2nd Department of Obstetrics and Gynecology Budapest Hungary

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G. Bekesi Semmelweis University and Department Geriatrics, National Institute of Psychiatry & Neurology 2nd Department of Internal Medicine — Department Section of Geriatrics, Faculty of Medicine Budapest Hungary

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E. Monos Semmelweis University and Department Geriatrics, National Institute of Psychiatry & Neurology Institute of Human Physiology and Clinical Experimental Research Budapest Hungary

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Szabolcs Várbíró

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Hypertension causes small vessel remodeling, vasomotor alterations. We investigated diameter, tone and mechanics of intramural small coronaries of female rats that received chronic angiotensin treatment to induce hypertension.Angiotensin II infusion (AII, 100 ng/bwkg/min, sc.) was used to establish hypertension in 10 female rats. Other 10 rats served as controls. Following 4 weeks of treatment, side branches of the left anterior descendant coronary (diameter∼200 μm) were isolated, cannulated and pressure-diameter curves were registered between 2–90 mmHg. Changes in vessel diameter were measured in Krebs solution, in the presence of thromboxane A2 receptor agonist (U46619, 10−6M), bradykinin (BK, 10−6M), and finally at complete relaxation (in Ca2+-free solution).Chronic AII treatment raised the mean arterial pressure (130±5 mmHg vs. 96±2 mmHg, average ±SEM) significantly. Wall thickness of the AII group was significantly greater (40.2±4.2 μm vs. 31.4±2.7 μm at 50 mmHg in Ca2+-free solution), but cross-section of the vessel wall did not differ. Tangentional wall stress and elastic modulus decreased significantly in hypertensive animals. Constrictions in the presence of U46619 were greater in the AII group (24.4± 5.6% vs. 14.5±3.3% at 50 mmHg).In hypertension, intramural small coronaries showed inward eutrophic remodeling, as a morphological adaptation following AII treatment enhanced thromboxane A2 — induced tone.

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Senior editors

Editor(s)-in-Chief: Rosivall, László

Honorary Editor(s)-in-Chief): Monos, Emil

Managing Editor(s): Bartha, Jenő; Berhidi, Anna

Co-editor(s): Koller, Ákos; Lénárd, László; Szénási, Gábor

Assistant Editor(s): G. Dörnyei (Budapest), Zs. Miklós (Budapest), Gy. Nádasy (Budapest)

Hungarian Editorial Board

    1. Benedek, György (Szeged)
    1. Benyó, Zoltán (Budapest)
    1. Boros, Mihály (Szeged)
    1. Chernoch, László (Debrecen)
    1. Détári, László (Budapest)
    1. Hamar, János (Budapest)
    1. Hantos, Zoltán (Szeged)
    1. Hunyady, László (Budapest)
    1. Imre, Sándor (Debrecen)
    1. Jancsó, Gábor (Szeged)
    1. Karádi, Zoltán (Pécs)
    1. Kovács, László (Debrecen)
    1. Palkovits, Miklós (Budapest)
    1. Papp, Gyula (Szeged)
    1. Pavlik, Gábor (Budapest)
    1. Spät, András (Budapest)
    1. Szabó, Gyula (Szeged)
    1. Szelényi, Zoltán (Pécs)
    1. Szolcsányi, János (Pécs)
    1. Szollár, Lajos (Budapest)
    1. Szücs, Géza (Debrecen)
    1. Telegdy, Gyula (Szeged)
    1. Toldi, József (Szeged)
    1. Tósaki, Árpád (Debrecen)

International Editorial Board

    1. R. Bauer (Jena)
    1. W. Benjelloun (Rabat)
    1. A. W. Cowley Jr. (Milwaukee)
    1. D. Djuric (Belgrade)
    1. C. Fry (London)
    1. S. Greenwald (London)
    1. O. Hänninen (Kuopio)
    1. H. G. Hinghofer-Szalkay (Graz)
    1. Th. Kenner (Graz)
    1. Gy. Kunos (Richmond)
    1. M. Mahmoudian (Tehran)
    1. T. Mano (Seki, Gifu)
    1. G. Navar (New Orleans)
    1. H. Nishino (Nagoya)
    1. O. Petersen (Liverpool)
    1. U. Pohl (Münich)
    1. R. S. Reneman (Maastricht)
    1. A. Romanovsky (Phoenix)
    1. G. M. Rubanyi (Richmond)
    1. T. Sakata (Oita)
    1. A. Siddiqui (Karachi)
    1. Cs. Szabo (Beverly)
    1. E. Vicaut (Paris)
    1. N. Westerhof (Amsterdam)
    1. L. F. Zhang (Xi'an)

Editorial Office:
Akadémiai Kiadó Zrt.
Prielle Kornélia u. 21–35, H-1117 Budapest, Hungary

Editorial Correspondence:
Acta Physiologica Hungarica
Semmelweis University, Faculty of Medicine Institute of Pathophysiology
Nagyvárad tér 4, H-1089 Budapest, Hungary
Phone/Fax: +36-1-2100-100
E-mail: aph@semmelweis-univ.hu

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Acta Physiologica Hungarica
Language English
Size  
Year of
Foundation
1950
Publication
Programme
changed title
Volumes
per Year
 
Issues
per Year
 
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 0231-424X (Print)
ISSN 1588-2683 (Online)

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