ArticleCardiovascular research2013
Prolonged vasoconstriction of resistance arteries involves vascular smooth muscle actin polymerization leading to inward remodelling.
Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 66 citations in OpenAlex.
- Trial
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- Guidelines for the measurement of vascular function and structure in isolated arteries and veins.American journal of physiology. Heart and circulatory physiology · 2021Review
- The cellular mechanobiology of aging: from biology to mechanics.Annals of the New York Academy of Sciences · 2021Review
- Microbiota Introduced to Germ-Free Rats Restores Vascular Contractility and Blood Pressure.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Regulation of smooth muscle contraction by monomeric non-RhoA GTPases.British journal of pharmacology · 2020Review
- LIMK (LIM Kinase) Inhibition Prevents Vasoconstriction- and Hypertension-Induced Arterial Stiffening and Remodeling.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Inhibition of Female and Male Human Detrusor Smooth Muscle Contraction by the Rac Inhibitors EHT1864 and NSC23766.Frontiers in pharmacology · 2020Article
- Formyl peptide receptor-1 activation exerts a critical role for the dynamic plasticity of arteries via actin polymerization.Pharmacological research · 2019Article
- Hypertension Induced Morphological and Physiological Changes in Cells of the Arterial Wall.American journal of hypertension · 2018Review
- α-Isocubebene modulates vascular tone by inhibiting myosin light chain phosphorylation in murine thoracic aorta.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
- Assessing Collagen and Elastin Pressure-dependent Microarchitectures in Live, Human Resistance Arteries by Label-free Fluorescence Microscopy.Journal of visualized experiments : JoVE · 2018Article
- Vascular smooth muscle contraction in hypertension.Cardiovascular research · 2018Review
- Redox regulation of the actin cytoskeleton and its role in the vascular system.Free radical biology & medicine · 2017Review
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
aimsInward remodelling of the resistance vasculature is predictive of hypertension and life-threatening cardiovascular events. We hypothesize that the contractile mechanisms responsible for maintaining a reduced diameter over time in response to prolonged stimulation with vasoconstrictor agonists are in part responsible for the initial stages of the remodelling process. Here we investigated the role of vascular smooth muscle (VSM) actin polymerization on agonist-induced vasoconstriction and development of inward remodelling. METHODS AND
resultsExperiments were conducted in Sprague-Dawley rat resistance vessels isolated from the cremaster and mesentery. Within blood vessels, actin dynamics of VSM were monitored by confocal microscopy after introduction of fluorescent actin monomers through electroporation and by differential centrifugation to probe globular (G) and filamentous (F) actin content. Results indicated that 4 h of agonist-dependent vasoconstriction induced inward remodelling and caused significant actin polymerization, elevating the F-/total-actin ratio. Inhibition of actin polymerization prevented vessels from maintaining prolonged vasoconstriction and developing inward remodelling. Activation of the small GTPases Rho/Rac/Cdc42 also increased the F-/total-actin ratio and induced inward remodelling, while inhibition of Rho kinase or Rac-1 prevented inward remodelling. Disruption of the actin cytoskeleton reversed the inward remodelling caused by prolonged vasoconstriction, but did not affect the passive diameter of freshly isolated vessels.
conclusionThese results indicate that vasoconstriction-induced inward remodelling is in part caused by the polymerization of actin within VSM cells through activation of small GTPases.
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