Effects of endothelin-11-31 on cell viabililty and [Ca2+]i in cultured neonatal rat cardiomyocytes

Title:

Effects of endothelin-11-31 on cell viabililty and [Ca2+]i in cultured neonatal rat cardiomyocytes
Effects of endothelin-11-31 on cell viability and [Ca2+]i in cultured neonatal rat cardiomyocytes

Creator:

Ren, A.-J., Yuan, X., Lin, Li, Pan, Y.-X., Qing, Y.-W., and Yuan, Wen-Jun

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:dfe4f7ca-56e2-4c59-8af4-946b16bf5ac1
uuid:dfe4f7ca-56e2-4c59-8af4-946b16bf5ac1
issn:0862-8408

Subject:

Experimentální medicína, fyziologie, potkan, vápník, physiology, Rattus norvegicus, calcium, endothelin-11-31, cardiomyocytes, 14, and 616-092

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

We previously found that Endothelin-11-31 (ET-11-31) exhibited a pro-arrhythmogenic effect in isolated rat hearts. In this study, we further investigated the effects of ET-11-31 on a cell viability and observed [Ca2+]i in cultured cardiomyocytes. Cultured neonatal rat cardiomyocytes were treated with 0.1, 1, and 10 nM ET-11-31 for 24h in the presence or absence of ETA receptor antagonist (BQ123) or phosphoramidon, a NEP/ECE inhibitor. Cell injury was evaluated by supernatant lactate dehydrogenase (LDH) assay, superoxide dismutase (SOD activity, and malondialdehyde (MDA) content. Cell viability was assessed by MTT assay. [Ca2+]i was measured with Fluo-3/AM under a laser confocal microscope. 1) ET-11-31 dose-dependently increased LDH release and decreased cell viability. 2) LDH and MDA levels were significantly elevated and SOD activity decreased after administration of 1 nM ET-11-31 for 24h, and these changes were markedly attenuated by 1 uM BQ123. 3) Exposure to 10 nM ET-11-31 caused a continuous increase in [Ca2+]i to cultured beating cardiomyocytes and termination of [Ca2+]i transient within 6 min, and this change was reversed by 1 uM BQ123 and attenuated by 0.5 mM phosphoramidon. These results suggest that ET-11-31 could cause cell injury, and that the effect of ET-11-31 on [Ca2+]i transients is mainly mediated by ETA receptor and partially attributed to the conversion of ET-11-31 to ET-11-21., A.-J. Ren, X. Yuan, L. Lin, Y.-X. Pan, Y.-W. Qing, W.-J. Yuan., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

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

Source:

Physiological research | 2008 Volume:57 | Number:3

Harvested from:

CDK

Metadata only:

false