ArticleExperimental diabetes research2012
5HT(2A) and 5HT(2B) receptors contribute to serotonin-induced vascular dysfunction in diabetes.
Article in Experimental diabetes research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 26 citations in OpenAlex.
- Serotonin Signaling and Vascular Reactivity in Cardiometabolic Disease and Cardiac Surgery.Cells · 2026Review
- Synergistic Interaction of 5-HTInternational journal of molecular sciences · 2023Article
- The serotonergic system dysfunction in diabetes mellitus.Frontiers in cellular neuroscience · 2022Review
- Saliva Proteomics Analysis Offers Insights on Type 1 Diabetes Pathology in a Pediatric Population.Frontiers in physiology · 2018Article
- Serotonin and Its Receptor as a New Antioxidant Therapeutic Target for Diabetic Kidney Disease.Journal of diabetes research · 2017Review
- Multiple activation mechanisms of serotonin-mediated contraction in the carotid arteries obtained from spontaneously hypertensive rats.Pflugers Archiv : European journal of physiology · 2016Article
- Insulin augments serotonin-induced contraction via activation of the IR/PI3K/PDK1 pathway in the rat carotid artery.Pflugers Archiv : European journal of physiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although 5HT(2A) receptors mediate contractions of normal arteries to serotonin (5HT), in some cardiovascular diseases, other receptor subtypes contribute to the marked increase in serotonin contractions. We hypothesized that enhanced contractions of arteries from diabetics to 5HT are mediated by an increased contribution from multiple 5HT receptor subtypes. We compared responses to selective 5HT receptor agonists and expression of 5HT receptor isoforms (5HT(1B), 5HT(2A), and 5HT(2B)) in aorta from nondiabetic (ND) compared to type 2 diabetic mice (DB, BKS.Cg-Dock7(m)+/+Lepr(db)/J). 5HT, 5HT(2A) (TCB2 and BRL54443), and 5HT(2B) (norfenfluramine and BW723C86) receptor agonists produced concentration-dependent contractions of ND arteries that were markedly increased in DB arteries. Neither ND nor DB arteries contracted to a 5HT(1B) receptor agonist. MDL11939, a 5HT(2A) receptor antagonist, and LY272015, a 5HT(2B) receptor antagonist, reduced contractions of arteries from DB to 5HT more than ND. Expression of 5HT(1B), 5HT(2A), and 5HT(2B) receptor subtypes was similar in ND and DB. Inhibition of rho kinase decreased contractions to 5HT and 5HT(2A) and 5HT(2B) receptor agonists in ND and DB. We conclude that in contrast to other cardiovascular diseases, enhanced contraction of arteries from diabetics to 5HT is not due to a change in expression of multiple 5HT receptor subtypes.
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