Chronic stress promotes the progression of pressure overload-induced cardiac dysfunction through inducing more apoptosis and fibrosis

Title:

Chronic stress promotes the progression of pressure overload-induced cardiac dysfunction through inducing more apoptosis and fibrosis

Creator:

Liu, W., Wang, X., Mei, Z., Gong, J., Gao, X., Zhao, Y., Ma, J., Xie, F., and Qian, L.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:65a129d1-7804-40ee-bb65-ce5fffeb4be2
uuid:65a129d1-7804-40ee-bb65-ce5fffeb4be2
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, stres (fyziologie), stress (physiology), chronic stress, pressure overload, cardiac dysfunction, norepinephrine, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Stress serves as a risk factor in the etiology of hypertension. The present study was designed to decipher the effect and mechanism of chronic stress on the progression of pressure overload-induced cardiac dysfunction. We used abdominal aortic constriction (AAC) to induce pressure overload with or without chronic restraint stress to establish the animal models. Echocardiographic analysis showed pressure overload-induced cardiac dysfunction was worsened by chronic stress. Compared with the AAC rats, there is a significant increase in cardiac hypertrophy, injury, apoptosis and fibrosis of the AAC + stress rats. Furthermore, we found the secretion of norepinephrine (NE) increased after the AAC operation, while the level of NE was higher in the AAC + stress group. Cardiomyocytes and cardiac fibroblasts isolated from neonatal rats were cultured and separately treated with 1, 10, 100 μM NE. The higher concentration NE induced more cardiomyocytes hypertrophy and apoptosis, cardiac fibroblasts proliferation and collagen expression. These results revealed that high level of NE-induced cardiomyocytes hypertrophy and apoptosis, cardiac fibroblasts proliferation and collagen expression further contributes to the effect of chronic stress on acceleration of pressure overloadinduced cardiac dysfunction., W. Liu, X. Wang, Z. Mei, J. Gong, X. Gao, Y. Zhao, J. Ma, F. Xie, L. Qian., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:3

Harvested from:

CDK

Metadata only:

false