ArticlePloS one2015
Relationship between human evolution and neurally mediated syncope disclosed by the polymorphic sites of the adrenergic receptor gene α2B-AR.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Analysis of adenylate cyclase activity in Japanese children with orthostatic dysregulation.PloS one · 2026Article
- Association of adenylate cyclase activity in vasopressor-type neurally mediated syncope based on the α2b-AR gene.PloS one · 2025Article
- Onset Mechanisms and Prognosis of Neurally Mediated Syncope.Reports (MDPI) · 2023Review
- Effects of Genetic Mutation Sites in ADR Genes on Modern Chickens Produced and Domesticated by Artificial Selection.Biology · 2023Article
- Genetic Analysis of Cardiac Syncope-Related Genes in Korean Patients with Recurrent Neurally Mediated Syncope.Journal of cardiovascular development and disease · 2022Article
- Clinical Significance of the Head-Up Tilt Test in Improving Prognosis in Patients with Possible Neurally Mediated Syncope.Biology · 2021Article
- Diagnosis and prevention of the vasodepressor type of neurally mediated syncope in Japanese patients.PloS one · 2021Article
- Analysis of the source of aggressiveness in gamecocks.Scientific reports · 2020Article
- Neurally mediated syncope diagnosis based on adenylate cyclase activity in Japanese patients.PloS one · 2019Article
- Urological dysfunction in synucleinopathies: epidemiology, pathophysiology and management.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2018Review
- Self-Organization of Blood Pressure Regulation: Clinical Evidence.Frontiers in physiology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to clarify the effects of disease on neurally mediated syncope (NMS) during an acute stress reaction. We analyzed the mechanism of the molecular interaction and the polymorphisms of the alpha-2 adrenoreceptor (α2B-AR) gene as the potential psychiatric cause of incentive stress. We focused on the following three genotypes of the repeat polymorphism site at Glu 301-303 in the α2B-AR gene: Glu12/12, Glu12/9, and Glu9/9. On the basis of our clinical research, NMS is likely to occur in people with the Glu12/9 heterotype. To verify this, we assessed this relationship with the interaction of Gi protein and adenylate cyclase by in silico analysis of the Glu12/9 heterotype. By measuring the difference in the dissociation time of the Gi-α subunit twice, we found that the Glu12/9 heterotype suppressed the action of adenylate cyclase longer than the Glu homotypes. As this difference in the Glu repeat number effect is thought to be one of the causes of NMS, we investigated the evolutionary significance of the Glu repeat number. Glu8 was originally repeated in simians, while the Glu12 repeats occurred over time during the evolution of bipedalism in humans. Taken with the Glu12 numbers, NMS would likely become a defensive measure to prevent significant blood flow to the human brain.
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