ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2010
Impaired feedback regulation of the receptor activity and the myofilament Ca2+ sensitivity contributes to increased vascular reactiveness after subarachnoid hemorrhage.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 30 citations in OpenAlex.
- PAR2 Regulates Cardiac Pressure and Vascular Function Through Context-Dependent Signalling Mechanisms.Current issues in molecular biology · 2026Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Secondary White Matter Injury and Therapeutic Targets After Subarachnoid Hemorrhage.Frontiers in neurology · 2021Review
- Mechanisms underlying TNFα-induced enhancement of force generation in airway smooth muscle.Physiological reports · 2019Article
- Myosin di-phosphorylation and peripheral actin bundle formation as initial events during endothelial barrier disruption.Scientific reports · 2016Article
- The single and double blood injection rabbit subarachnoid hemorrhage model.Translational stroke research · 2015Review
- The vascular clock system generates the intrinsic circadian rhythm of vascular contractility.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2015Review
- The rabbit blood-shunt model for the study of acute and late sequelae of subarachnoid hemorrhage: technical aspects.Journal of visualized experiments : JoVE · 2014Article
- Upregulation of relaxin after experimental subarachnoid hemorrhage in rabbits.BioMed research international · 2014Article
- Contribution of PGE2 EP1 receptor in hemin-induced neurotoxicity.Frontiers in molecular neuroscience · 2013Article
- Mechanisms underlying potentiation of endothelin-1-induced myofilament Ca(2+) sensitization after subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Article
- Combined argatroban and anti-oxidative agents prevents increased vascular contractility to thrombin and other ligands after subarachnoid haemorrhage.British journal of pharmacology · 2012Article
- Putative role of prostaglandin receptor in intracerebral hemorrhage.Frontiers in neurology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral vasospasm determines the prognosis of subarachnoid hemorrhage (SAH). The increased vascular reactiveness has an important role in the development of cerebral vasospasm. This study analyzed the roles of the receptor-mediated signaling and the myofilament Ca(2+) sensitivity in the increased vascular reactiveness in SAH, using the basilar artery of a rabbit SAH model. Endothelin-1, thrombin, and phenylephrine induced transient increases in [Ca(2+)](i), myosin light chain phosphorylation, and contraction in the controls. All these responses were not only enhanced but also became sustained in SAH. In the sequential stimulation of thrombin receptor or alpha(1)-adrenoceptor, the second response was substantially attenuated in the controls, whereas it was maintained in SAH. The thrombin-induced contraction in SAH irreversibly persisted even after terminating the thrombin stimulation. This contraction was completely reversed by trypsin and a Galpha(q) inhibitor YM254890, thus suggesting the sustained receptor activity during the sustained contraction. YM254890 also inhibited the endothelin-1- and phenylephrine-induced sustained contraction. Furthermore, the GTPgammaS-induced transient contraction in the control alpha-toxin-permeabilized strips was converted to a sustained contraction in SAH. The results provide the first evidence that the feedback inactivation of the receptor activity and the myofilament Ca(2+) sensitivity was impaired in SAH, thus contributing to the increased vascular reactiveness.
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.