ArticleNaunyn-Schmiedeberg's archives of pharmacology2004
Calcium channel function and regulation in beta 1- and beta 2-adrenoceptor transgenic mice.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2004. 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Opposite effects of GαNaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice.Cardiovascular research · 2015Article
- Article
- beta-adrenoceptors and potassium channels.Naunyn-Schmiedeberg's archives of pharmacology · 2006Article
- Calcium channel function and regulation in beta 1- and beta 2-adrenoceptor transgenic mice.Naunyn-Schmiedeberg's archives of pharmacology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac effects of catecholamines on the L-type calcium channel depend on beta-adrenoceptor subtype (beta(1)- vs. beta(2)-adrenoceptor). Chronic overexpression of these receptors leads to hypertrophy and early death at moderate (beta(1)) or excessive (beta(2)) levels of overexpression respectively. In order to examine the role of L-type calcium channels in altered cardiomyocyte calcium homeostasis found with beta(1)-adrenoceptor overexpression, and to understand the quantitative differences between beta-adrenoceptor subtypes regarding calcium channel regulation, we examined single channels in myocytes obtained from beta(1)- and beta(2)-adrenoceptor transgenic mice. The effects of the agonist isoproterenol were investigated and compared with acute receptor stimulation in the respective non-transgenic littermates. Channels from beta(1)-adrenoceptor transgenic mice have normal baseline activity, and channel number is not reduced. This contrasts to previous findings with beta(2)-adrenoceptor transgenic mice, where channel activity is depressed. Isoproterenol is unable to stimulate channel activity in both transgenic models. In conclusion, the L-type calcium channel is not likely to be involved in alterations of calcium handling of beta(1)-adrenoceptor transgenic myocytes. Furthermore, chronic beta(1)-adrenoceptor overexpression does not depress channel activity, giving another example of the difference between beta(1)- and beta(2)-adrenoceptor signal transduction.
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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 OpenQuestion graph.