ArticleHeart and vessels2012
Endothelin-1 prolongs intracellular calcium transient decay in neonatal rat cardiac myocytes.
Article in Heart and vessels, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- A gene regulatory element modulates myosin expression and controls cardiomyocyte response to stress.Genome research · 2025Article
- GABAB receptors are expressed in human aortic smooth muscle cells and regulate the intracellular Ca(2+) concentration.Heart and vessels · 2015Article
- Heart rate reduction with ivabradine prevents thyroid hormone-induced cardiac remodeling in rat.Heart and vessels · 2013Article
- The association between clinical symptoms, laboratory findings and serum endothelin 1 concentrations, in cirrhotic patients with and without hepatopulmonary syndrome.Gastroenterology and hepatology from bed to bench · 2012Article
- [Effects of propofol pretreatment on myocardial cell apoptosis and SERCA2 expression in rats with hepatic ischemia/reperfusion].Brazilian journal of anesthesiology (Elsevier)Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelin-1 (ET-1) is involved in the development of cardiac hypertrophy and heart failure. We investigated the effects of ET-1 on intracellular calcium transient and its mechanisms. Neonatal rat cardiomyocytes were prepared and calcium transient was measured using fura-2. Treatment with ET-1 for 48 h prolonged calcium transient decay. In the presence of thapsigargin, ET-1 did not alter calcium transient decay. On the other hand, the prolonged calcium transient decay was maintained even when sodium was removed from the bath solution. These results indicate that ET-1-induced prolongation of calcium transient decay is mainly due to the suppression of calcium uptake by sarcoplasmic reticulum, but not inhibition of the sodium/calcium exchanger. Northern blotting analysis revealed that sarcoplasmic reticulum ATPase (SERCA2) mRNA was decreased in ET-1-treated cardiomyocytes, and that this decrease was inhibited by BQ-123 but not by BQ-788. Moreover, pretreatment with chelerythrine partially restored the ET-1-induced decrease in SERCA2 mRNA, whereas phorbol 12-myristate 13-acetate markedly reduced SERCA2 gene expression. Real-time RT-PCR analysis showed abundant ETA receptor gene expression in cardiomyocytes. ET-1 reduces SERCA2 gene expression through the ETA receptor and PKC pathway, and prolongs intracellular calcium transient decay. Specific inhibition of the ETA receptor may be a possible therapeutic strategy for improving cardiac performance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.