Acta Physiologica Hungarica
Volume/Issue:
Volume 103: Issue 2
Alterations of store-operated calcium entry and cyclopiazonic acid-induced endothelium-derived relaxations in aging rat thoracic aorta
Authors:
Y Erac Department of Pharmacology, Faculty of Pharmacy, Ege University, Izmir, Turkey

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C Selli Department of Pharmacology, Faculty of Pharmacy, Ege University, Izmir, Turkey

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M Tosun Department of Pharmacology, School of Medicine, Izmir University of Economics, Izmir, Turkey

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Pages:
146–156
Online Publication Date:
30 Jun 2016
Publication Date:
01 Jun 2016
Article Category:
Journal Article
DOI:
https://doi.org/10.1556/036.103.2016.2.2
Keywords:
aging; vascular responses; SOCE; endothelial dysfunction; TRPC
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The purpose of our study was to investigate whether endothelium-derived relaxations induced by store depletion are altered in aging rat thoracic aorta. Vascular responses were measured in aortic segments isolated from young (2–4 month) and old (20–24 month) male Sprague-Dawley rats. In phenylephrine-contracted intact tissues, receptor-mediated and receptor-independent endothelium-derived relaxations were induced by acetylcholine (ACh) and sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) blocker cyclopiazonic acid (CPA), respectively. In addition, CPA-induced changes in intracellular calcium levels were monitored in fura-2-loaded endothelium-denuded tissues. Real-time quantitative reverse transcription polymerase chain reaction and western blot analysis were performed to determine the transient receptor potential canonical (TRPC) 4 mRNA and protein levels. Endothelial TRPC4 mRNA levels were apparently decreased in aging rats. Immunoblot analysis showed that TRPC4 protein levels significantly decreased in intact aorta from 20- to 24-month-old rats compared to that from 2- to 4-month-old rats. ACh- and CPA-induced endothelium-dependent relaxations decreased in old rat aorta without any change in direct vasodilation induced by sodium nitroprusside. Store-operated Ca2+ entry (SOCE) induced by CPA was significantly decreased, whereas sarcoplasmic reticulum Ca2+ release was unaffected in endothelium-denuded aging rat aorta. In conclusion, TRPC4 downregulation could be associated with decreased endothelium-dependent vasorelaxations. As endothelial nitric oxide synthase is activated by SOCE-induced caveolar internalization, tracking the expression levels of SERCA, ion channels, and/or associated proteins involved in SOCE would lead to the development of novel therapeutics for age-related vasospastic disorders with dysfunctional endothelium.

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Cover Acta Physiologica Hungarica
Acta Physiologica Hungarica
Print ISSN:
0231-424X
Online ISSN:
1588-2683

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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