Adaptation of the heart to hypertension is associated with maladaptive gap junction connexin-43 remodeling

Title:

Adaptation of the heart to hypertension is associated with maladaptive gap junction connexin-43 remodeling

Creator:

Marcela Fialová, Katarína Dlugošová, Ľudmila Okruhlicová, Kristek, F., Manoach, M., and Narcisa Tribulová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:5332a853-207a-4084-b2e1-83c213cea893
uuid:5332a853-207a-4084-b2e1-83c213cea893
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie, hypertenze, srdeční arytmie, physiology, hypertension, cardiac arrhythmia, gap junction remodeling, connexin-43, malignant arrhythmias, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

We hypothesized that hypertension-related myocardial remodeling characterized by hypertrophy and fibrosis might be accompanied by cell-to-cell gap junction alterations that may account for increased arrhythmogenesis. Intercellular junctions and expression of gap junction protein connexin-43 were analyzed in rat heart tissues from both spontaneous (SHR) and L-NAME model of hypertension. Isolated heart preparation was used to examine susceptibility of the heart to lethal ventricular fibrillation induced by low potassium perfusion. Ultrastructure observation revealed enhanced neoformation of side-to-side type while internalization of end-to-end type (intercalated disc-related) of gap junctions prevailed in the myocardium of rats suffering from either spontaneous or L-NAME-induced hypertension. In parallel, immunolabeling showed increased number of connexin-43 positive gap junctions in lateral cell membrane surfaces, particularly in SHR. Besides, focal loss of immunopositive signal was observed more frequently in hearts of rats treated with L-NAME. There was a significantly higher incidence of hypokalemia-induced ventricular fibrillation in hypertensive compared to normotensive rat hearts. We conclude that adaptation of the heart to hypertension-induced mechanical overload results in maladaptive gap junction remodeling that consequently promotes development of fatal arrhythmias., M. Fialová, K. Dlugošová, L. Okrouhlicová, F. Kristek, M. Manoach, N. Tribulová., and Obsahuje bibliografii a biblioigrafické údaje

Language:

English

Rights:

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

Source:

Physiological research | 2008 Volume:57 | Number:1

Harvested from:

CDK

Metadata only:

false