J 2007

Modulation of expression of Na+/Ca2+ exchanger in heart of rat and mouse under stress

HUDECOVÁ, Soňa, Lucia KUBOVČÁKOVÁ, Richard KVETŇANSKÝ, Juraj KOPÁČEK, Silvia PASTOREKOVÁ et. al.

Basic information

Original name

Modulation of expression of Na+/Ca2+ exchanger in heart of rat and mouse under stress

Name in Czech

Modulace exprese Na+/Ca2+ výměníku za stresu u srdce potkana a myši

Authors

HUDECOVÁ, Soňa (703 Slovakia), Lucia KUBOVČÁKOVÁ (703 Slovakia), Richard KVETŇANSKÝ (703 Slovakia), Juraj KOPÁČEK (703 Slovakia), Silvia PASTOREKOVÁ (703 Slovakia), Marie NOVÁKOVÁ (203 Czech Republic, guarantor), Václav KNEZL (703 Slovakia), Bohuslava TARABOVÁ (703 Slovakia), Ľubica LACINOVÁ (703 Slovakia), Zdena SULOVÁ (703 Slovakia), Albert BREIER (703 Slovakia), Dana JURKOVIČOVÁ (703 Slovakia) and Olga KRIŽANOVÁ (703 Slovakia)

Edition

Acta Physiologica, Oxford, Blackwell Publishing, 2007, 1748-1708

Other information

Language

English

Type of outcome

Article in a journal

Field of Study

30105 Physiology

Country of publisher

Sweden

Confidentiality degree

is not subject to a state or trade secret

Impact factor

Impact factor: 1.602

RIV identification code

RIV/00216224:14110/07:00032320

Organization unit

Faculty of Medicine

UT WoS

000247565400005

Keywords in English

catecholamines;hypoxia;rat and mouse heart;sodium-calcium

Tags

Tags

International impact, Reviewed
Changed: 2/4/2010 10:45, prof. MUDr. Marie Nováková, Ph.D.

Abstract

ORIG CZ

V originále

Aim: The Na+/Ca2+ exchanger (NCX) is a major Ca2+ extrusion system in the plasma membrane of cardiomyocytes and an important component participating on the excitation-contraction coupling process in muscle cells. NCX1 isoform is the most abundant in the heart and is known to be changed after development of ischaemia or myocardial infarction. Objective of this study was to investigate the effect of stress factors (immobilization, cold and short-term hypoxia) on the expression of NCX1, in vivo, in the heart of rat and mouse. Methods: We compared gene expression and protein levels of control and stressed animals. The activity of NCX was measured by the whole cell configuration using the patch clamp. We also measured physiological parameters of the heart in physiological conditions and under ischaemiareperfusion to compare response of control and stressed hearts. Results: We have found that only strong stress stimulus (hypoxia, immobilization) applied repeatedly for several days elevated the NCX1 mRNA level. Cold, which is a weaker stressor that activates mainly sympathoneural, and only marginally adrenomedullary system did not affect the gene expression of NCX1. Thus, from these results it appears that hormones produced by the adrenal medulla (mainly adrenaline) might be involved in this process. To study possible mechanism of the NCX1 regulation by stress, we focused on the possible role of the hypothalamo-pituitary-adrenocortical pathway in the activation of catecholamine synthesis in the adrenal medulla. We have already published that cortisol affects activity, but not the gene expression of NCX1. In this work, we used corticotropin-releasing hormone (CRH) knockout mice, where secretion of corticosterone and subsequently adrenaline is significantly suppressed. As no increase in NCX1 mRNA was observed in CRH knockout mice due to immobilization stress, we proposed that adrenaline (probably regulated via corticosterone) is involved in the regulation of NCX1 gene expression during stress. Conclusions: The gene expression and protein levels of the NCX1 are increased by the strong stress stimuli, e.g. hypoxia, or immobilization stress. The activity of NCX1 is decreased. Based on these results, we assume that the gene expression of NCX is increased as a consequence of suppressed activity of this transport system.