Expression of catechol-O-methyltransferase (Comt), mineralocorticoid receptor (Mlr), and epithelial sodium channel (ENaC) genes in kidneys of hypertensive ISIAH rats at rest and during response to stress


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Resumo

Emotional stress plays a significant role in the processes of the development of arterial hypertension, especially in the presence of genetic predisposition. The origin and maintenance of hypertensive status during stress development can be activated by the sympathetic nervous system. An increase in sympathetic stimulation can, in turn, result in a change in the functions of kidneys, which provide fluid and electrolyte balance of the organism. A comparative study of the mRNA expression level of catechol-o-methyltransferase (Comt), mineralocorticoid receptor (Mlr), and β-subunit of epithelial sodium channel (β-ENaC) genes was conducted on the kidneys of hypertensive ISIAH rats and normotensive WAG rats at rest and after the effect of emotional stress. The discovered changes in the expression level of the selected genes confirm their involvement in increased sympathetic stimulation of the kidney, along with changes in the function of kidney regulation of fluid and electrolyte balance, which is an important factor of the development of sustained hypertension in the ISIAH rats strain.

Sobre autores

T. Abramova

Federal Research Center Institute of Cytology and Genetics, Siberian Branch

Autor responsável pela correspondência
Email: icg-adm@bionet.nsc.ru
Rússia, Novosibirsk, 630090

S. Smolenskaya

Federal Research Center Institute of Cytology and Genetics, Siberian Branch

Email: icg-adm@bionet.nsc.ru
Rússia, Novosibirsk, 630090

E. Antonov

Federal Research Center Institute of Cytology and Genetics, Siberian Branch

Email: icg-adm@bionet.nsc.ru
Rússia, Novosibirsk, 630090

O. Redina

Federal Research Center Institute of Cytology and Genetics, Siberian Branch

Email: icg-adm@bionet.nsc.ru
Rússia, Novosibirsk, 630090

A. Markel

Department of Physiology

Email: icg-adm@bionet.nsc.ru
Rússia, Novosibirsk, 630090


Declaração de direitos autorais © Pleiades Publishing, Inc., 2016

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