ReviewWiener medizinische Wochenschrift (1946)2006
[On the function of beta3-adrenoceptors in the human heart: signal transduction, inotropic effect and therapeutic prospects].
Review in Wiener medizinische Wochenschrift (1946), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Therapeutic Potential of the β3-Adrenergic Receptor and Its Ligands in Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- Pharmacology of myocardial calcium-handling.Wiener medizinische Wochenschrift (1946) · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta-adrenergic stimulation is an important regulatory mechanism of cardiac function. Next to beta1- and beta2-adrenoceptors, the expression of a third beta-adrenoceptor population, the beta3-adrenoceptor, has recently been evidenced in the human heart. Stimulation of cardiac beta3-adrenoceptors leads to a decrease in contractility via a release of nitric oxide (NO). In this context, different molecular mechanisms of endothelial nitric oxide synthase (eNOS) activation have been uncovered to occur as a consequence of beta3-adrenergic stimulation. In both nonfailing and failing myocardium, beta3-adrenergic stimulation may have a protective effect against excessive chatecolaminergic stimulation as it occurs during somatic and mental stress and during heart failure. For this reason, the beta3-adrenoceptor is discussed as a possible target for the pharmacological therapy of heart failure.
Indexed as
Identifiers
What OpenQuestion holds
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.