Integrins, vascular remodeling, and hypertension.
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Summary
Detailed structural and mechanical analyses have shown that eutrophic inward remodeling can narrow the vascular lumen without precipitating hypertrophy, and the reasons why resistance arteries respond to hypertension in this manner are considered.
- Type
- article
- Published
- 2007-01-01
- Cited by
- 96
- References
- 48
- Access
- Open access
- OpenAlex
- https://openalex.org/W17145983
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:858620
Keywords
Geography
References
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- Morphology and function of mesenteric resistance arteries in transgenic rats with low-renin hypertension
- Focal adhesion kinase: in command and control of cell motility
- Remodelling and Enhanced Myogenic Tone in Cerebral Resistance Arteries Isolated from Genetically Hypertensive Brattleboro Rats
- Effect of antihypertensive treatment on small arteries of patients with previously untreated essential hypertension.
- Extracellular matrix controls myosin light chain phosphorylation and cell contractility through modulation of cell shape and cytoskeletal prestress.
- Targeting of αv integrins interferes with FAK activation and smooth muscle cell migration and invasion
- Acute mechanoadaptation of vascular smooth muscle cells in response to continuous arteriolar vasoconstriction: implications for functional remodeling
- Small Artery Remodeling Depends on Tissue-Type Transglutaminase
- &agr;V Integrins Are Necessary for Eutrophic Inward Remodeling of Small Arteries in Hypertension
- Integrins control motile strategy through a Rho–cofilin pathway
- Regulation of the L-type calcium channel by alpha 5beta 1 integrin requires signaling between focal adhesion proteins.
- Different Involvement of Extracellular Matrix Components in Small and Large Arteries During Chronic NO Synthase Inhibition
- Cross-Linking Vasomotor Tone and Vascular Remodeling: A Novel Function for Tissue Transglutaminase?
- Persistent Remodeling of Resistance Arteries in Type 2 Diabetic Patients on Antihypertensive Treatment
- Imaging remodeling of the actin cytoskeleton in vascular smooth muscle cells after mechanosensitive arteriolar constriction.
Cited by
- Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage.
- Rôle des phophodiestérases dans la compartimentation subcellulaire de l'AMPc dans la cellule musculaire lisse vasculaire : étude des altérations dans l'insuffisance cardiaque
- Role of nitric oxide and prostanoids in the regulation of leg blood flow and blood pressure in humans with essential hypertension: effect of high‐intensity aerobic training
- Hypertension in Autosomal Dominant Polycystic Kidney Disease: A Clinical and Basic Science Perspective
- Deciphering actin cytoskeletal function in the contractile vascular smooth muscle cell
- Structural alterations in small resistance arteries in obesity.
- Direkte Reninhemmer oder Kirene
- Coordinated regulation of vascular Ca2+ and K+ channels by integrin signaling.
- The Dynamic Structure of Arterioles
- Retinal Arterial Hypertrophy: the New LVH?
- Relationship of left atrial enlargement to persistence or development of ECG left ventricular hypertrophy in hypertensive patients: implications for the development of new atrial fibrillation
- Action of ANP on the nongenomic dose-dependent biphasic effect of aldosterone on NHE1 in proximal S3 segment.
- Small artery structure and function in hypertension
- Hypertension and cerebrovascular dysfunction.
- Recent advances in arterial stiffness and wave reflection in human hypertension.
- A role for actin polymerization in persistent pulmonary hypertension of the newborn.
- Hypertension impairs myocardin function: a novel mechanism facilitating arterial remodelling.
- N-acetyl-seryl-aspartyl-lysyl-proline prevents cardiac remodeling and dysfunction induced by galectin-3, a mammalian adhesion/growth-regulatory lectin.
- Arterial stiffness, pulse pressure, and cardiovascular disease-is it possible to break the vicious circle?
- Mechanisms of the inward remodeling process in resistance vessels: Is the actin cytoskeleton involved?
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