ArticleFrontiers in physiology2014
Emerging trend in second messenger communication and myoendothelial feedback.
Article in Frontiers in physiology, 2014. 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.
- Myoendothelial feedback in mouse mesenteric resistance arteries is similar between the sexes, dependent on nitric oxide synthase, and independent of TPRV4.American journal of physiology. Heart and circulatory physiology · 2024Article
- Cyclooxygenase-dependent mechanisms mediate in part the anti-dilatory effects of perivascular adipose tissue in uterine arteries from pregnant rats.Pharmacological research · 2021Article
- Vasoconstrictor stimulus determines the functional contribution of myoendothelial feedback to mesenteric arterial tone.The Journal of physiology · 2018Article
- Vascular structural and functional changes: their association with causality in hypertension: models, remodeling and relevance.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Review
- Microtubule-Associated Protein EB3 Regulates IP3 Receptor Clustering and Ca(2+) Signaling in Endothelial Cells.Cell reports · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past decade, second messenger communication has emerged as one of the intriguing topics in the field of vasomotor control. Of particular interest has been the idea of second messenger flux from smooth muscle to endothelium initiating a feedback response that attenuates constriction. Mechanistic details of the precise signaling cascade have until recently remained elusive. In this perspective, we introduce readers to how myoendothelial gap junctions could enable sufficient inositol trisphosphate flux to initiate endothelial Ca(2+) events that activate Ca(2+) sensitive K(+) channels. The resulting hyperpolarizing current would in turn spread back through the same myoendothelial gap junctions to moderate smooth muscle depolarization and constriction. In discussing this defined feedback mechanism, this brief manuscript will stress the importance of microdomains and of discrete cellular signaling.
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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.