scholarly journals Vascular Remodeling in Experimental Hypertension

2005 ◽  
Vol 5 ◽  
pp. 959-971 ◽  
Author(s):  
Norma R. Risler ◽  
Montserrat C. Cruzado ◽  
Roberto M. Miatello
Keyword(s):  
Vascular Remodeling ◽  
Structural Changes ◽  
Peripheral Resistance ◽  
Vascular Wall ◽  
Secondary Hypertension ◽  
Experimental Models ◽  
Experimental Hypertension ◽  
Vascular Protection ◽  
The Metabolic Syndrome ◽  
Extracellular Matrix Components

The basic hemodynamic abnormality in hypertension is an increased peripheral resistance that is due mainly to a decreased vascular lumen derived from structural changes in the small arteries wall, named (as a whole) vascular remodeling. The vascular wall is an active, flexible, and integrated organ made up of cellular (endothelial cells, smooth muscle cells, adventitia cells, and fibroblasts) and noncellular (extracellular matrix) components, which in a dynamic way change shape or number, or reorganize in response to physiological and pathological stimuli, maintaining the integrity of the vessel wall in physiological conditions or participating in the vascular changes in cardiovascular diseases such as hypertension. Research focused on new signaling pathways and molecules that can participate in the mechanisms of vascular remodeling has provided evidence showing that vascular structure is not only affected by blood pressure, but also by mechanisms that are independent of the increased pressure. This review will provide an overview of the evidence, explaining some of the pathophysiologic mechanisms participating in the development of the vascular remodeling, in experimental models of hypertension, with special reference to the findings in spontaneously hypertensive rats as a model of essential hypertension, and in fructose-fed rats as a model of secondary hypertension, in the context of the metabolic syndrome. The understanding of the mechanisms producing the vascular alterations will allow the development of novel pharmacological tools for vascular protection in hypertensive disease.

scholarly journals THE ROLE OF VASCULAR REMODELING IN THE FORMATION OF STRUCTURAL PHENOTYPES OF OSTEOARTHRITIS

2018 ◽  
Vol 25 (3) ◽  
pp. 61-67
Author(s):  
M. A. KABALYK ◽  
V. A. NEVZOROVA
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Knee Joint ◽  
Vascular Remodeling ◽  
Structural Changes ◽  
Vascular Wall ◽  
External Diameter ◽  
Resonance Imaging ◽  
Structural Progression

Aim. Evaluation of the role of vascular remodeling in the formation of structural phenotypes of osteoarthritis (OA).Materials and methods. 62 patients with OA aged 65,9±8,8 years and 18 volunteers without clinical and roentgenologic signs of OA aged 60,7±7,9 years were examined. All patients underwent magnetic resonance imaging of knee joints. To analyze the structural changes in the tissues of the knee joint, the WORMS protocol was used for magnetic resonance imaging. The thickness of the vascular wall, the external diameter, the vascular index (VI) were measured – the ratio of the diameter of the lumen of the vessel to the thickness of the popliteal artery (PA) wall, the branch of the upper lateral artery (LA), the medial artery of the knee (MA).Results. The analysis of the parameters of the arteries of the knee joint showed that with a subchondral OA phenotype, the thickness of the PA wall is statistically significantly larger than the cartilage phenotype, and the vascular index of the PA is significantly higher in the group of the cartilaginous phenotype. The upper LA wall was significantly thicker in the subchondral OA phenotype. VI of the upper LA was significantly lower in patients with a subchondral phenotype compared with the cartilaginous phenotype. The thickness of the MA wall was also larger with a bone phenotype, and VI with a cartilaginous phenotype.Conclusion. The results of the study showed the relationship between vascular remodeling and structural progression of OA. Changes in the vascular wall adversely affect all joint tissues, leading to their remodeling. It was established that the degree of vascular remodeling determines the formation of structural OA phenotypes. Severe vascular changes are associated with the subchondral OA phenotype.

Model Characterization of Pulmonary Arterial Hypertension: Analysis of Lung Pathology with Respect to Human Disease

2020 ◽  
Author(s):  
◽  
Eptisam lambu
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Human Disease ◽  
Vascular Remodeling ◽  
Vascular Wall ◽  
Lung Pathology ◽  
Pulmonary Arterial ◽  
Lung Pathogenesis ◽  
Arterial Endothelial Cells

Pulmonary arterial hypertension (PAH) is a rare multifactorial disease characterized by abnormal high blood pressure in the pulmonary artery, or increased pulmonary vascular resistance (PVR), caused by obstruction in the small arteries of the lung. Increased PVR is also thought to be caused by abnormal vascular remodeling, due to thickening of the pulmonary vascular wall resulting from significant hypertrophy of pulmonary arterial smooth-muscle cells (PASMCs) and increased proliferation/impaired apoptosis of pulmonary arterial endothelial cells (PAECs). Herein, we investigated the mechanisms and explored molecular pathways mediating the lung pathogenesis in two PAH rat models: Monocrotaline (MCT) and Sugen5416/Hypoxia (SuHx). We analyzed these disease models to determine where the vasculature shows the most severe PAH pathology and which model best recapitulates the human disease. We investigated the role vascular remodeling, hypoxia, cell proliferation, apoptosis, DNA damage and inflammation play in the pathogenesis of PAH. Neither model recapitulated all features of the human disease, however each model presented with some of the pathology seen in PAH patients.

Perspectives on endothelial-to-mesenchymal transition: potential contribution to vascular remodeling in chronic pulmonary hypertension

2007 ◽  
Vol 293 (1) ◽  
pp. L1-L8 ◽  
Author(s):  
Enrique Arciniegas ◽  
Maria G. Frid ◽  
Ivor S. Douglas ◽  
Kurt R. Stenmark
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Vascular Remodeling ◽  
Serine Proteases ◽  
Structural Changes ◽  
Transforming Growth Factor ◽  
Pulmonary Arteries ◽  
Potential Contribution ◽  
Mesenchymal Transition ◽  
Endothelial Mesenchymal Transition

All forms of pulmonary hypertension are characterized by structural changes in pulmonary arteries. Increased numbers of cells expressing α-smooth muscle (α-SM) actin is a nearly universal finding in the remodeled artery. Traditionally, it was assumed that resident smooth muscle cells were the exclusive source of these newly appearing α-SM actin-expressing cells. However, rapidly emerging experimental evidence suggests other, alternative cellular sources of these cells. One possibility is that endothelial cells can transition into mesenchymal cells expressing α-SM actin and that this process contributes to the accumulation of SM-like cells in vascular pathologies. We review the evidence that endothelial-mesenchymal transition is an important contributor to cardiac and vascular development as well as to pathophysiological vascular remodeling. Recent work has provided evidence for the role of transforming growth factor-β, Wnt, and Notch signaling in this process. The potential roles of matrix metalloproteinases and serine proteases are also discussed. Importantly, endothelial-mesenchymal transition may be reversible. Thus insights into the mechanisms controlling endothelial-mesenchymal transition are relevant to vascular remodeling and are important as we consider new therapies aimed at reversing pulmonary vascular remodeling.

RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats

1996 ◽  
Vol 271 (2) ◽  
pp. H602-H613 ◽  
Author(s):  
M. P. Kunert ◽  
J. F. Liard ◽  
D. J. Abraham
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Experimental Models ◽  
Metabolic Demand ◽  
Flow Probe ◽  
Inositol Hexaphosphate ◽  
Control Value ◽  
Allosteric Effector

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

scholarly journals STRUCTURAL CHANGES IN THE MICROCIRCULATORY BED OF THE PANCREAS IN RATS WITH EXPERIMENTAL METABOLIC SYNDROME

2018 ◽  
Vol 15 (3) ◽  
pp. 347-353
Author(s):  
T. E. Kuznetsova ◽  
E. L. Ryzhkovskaya ◽  
E. I. Kalinovskaya
Keyword(s):  
Metabolic Syndrome ◽  
Glucose Oxidation ◽  
Structural Changes ◽  
Krebs Cycle ◽  
Electron Microscopic ◽  
Microcirculatory Bed ◽  
The Metabolic Syndrome ◽  
Marginal State ◽  
Inflammatory Changes ◽  
Blood Elements

A complex histological, histochemical and electron microscopic study of the state of the microcirculatory bed of the pancreas and conjugate transformations in the parenchyma of the organ after modeling the metabolic syndrome using a diet high in fats and carbohydrates was carried out. Spasm of arterioles, the marginal state of leukocytes and the desquamation of endotheliocytes into the lumen of a vessel, the stasis of erythrocytes in capillaries were revealed. The endothelial cells of capillaries had signs of increased transport of substances through the vessel walls: pinocytosis, fenestration, loosening of basal membranes. It was observed that capillaries are filled with shaped blood elements, on the luminal surface of endotheliocytes nuclei are protruded and the cytoplasm outgrowth into the lumen of the vessel is formed. At the same time, glucose oxidation accelerated both in the Krebs cycle and along the glycolytic pathway in the endotheliocytes of the vessels of the microcirculatory bed, indicating that the energy was supplied to the cells at a higher level. Disturbances of microcirculation were accompanied by focal destructive and inflammatory changes in the parenchyma of the organ.

Spectroscopic evaluation of painted layer structural changes induced by gamma radiation in experimental models

2012 ◽  
Vol 81 (2) ◽  
pp. 160-167 ◽  
Author(s):  
Mihaela M. Manea ◽  
Ioan V. Moise ◽  
Marian Virgolici ◽  
Constantin D. Negut ◽  
Olimpia-Hinamatsuri Barbu ◽  
...  
Keyword(s):  
Gamma Radiation ◽  
Structural Changes ◽  
Experimental Models ◽  
Painted Layer

CALCIUM AND VITAMIN : EFFECTS ON BONE TISSUE AND VASCULAR REMODELING (LITERATURE REVIEW)

2021 ◽  
pp. 1200-1208
Author(s):  
С. В. Булгакова ◽  
Е. В. Тренева ◽  
Н. О. Захарова ◽  
А. В. Николаева
Keyword(s):  
Literature Review ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Vascular Wall ◽  
Arterial Calcification ◽  
Mineral Density ◽  
Treatment And Prevention ◽  
Calcium Deposits ◽  
Local Accumulation ◽  
Progression Of Atherosclerosis

Препараты кальция входят в схемы лечения и профилактики низкой минеральной плотности костной ткани. Однако последние научные исследования показали, что дополнительное поступление кальция может увеличить риск сердечно-сосудистых заболеваний. Это связано с отложением кальция в эндотелии кровеносных сосудов. Значимость минерализации сосудистой стенки не ограничивается локальным накоплением кальциевых депозитов, но в значительной мере определяется их активирующим влиянием на прогрессирование атеросклероза. Витамин К играет важную роль в гомеостазе кальция, снижает артериальную кальцификацию и артериальную жесткость и, как следствие, оказывает протективный эффект при приеме кальция. В данном обзоре литературы представлена современная информация о кальциевом парадоксе, обсуждаются основные молекулярные механизмы кальцификации сосудов, рассмотрены терапевтические стратегии лечения витамином К . Calcium preparations are included in the treatment and prevention regimens for low bone mineral density. However, recent scientific studies have shown that additional calcium intake can increase the risk of heart disease, which is associated with the deposition of calcium in the endothelium of blood vessels. The significance of vascular wall mineralization is not limited to local accumulation of calcium deposits, but is largely determined by their activating effect on the progression of atherosclerosis. Vitamin K plays an important role in calcium homeostasis, reduces arterial calcification and arterial stiffness and, as a result, has a protective effect when taking calcium. This literature review provides current information about the calcium paradox, discusses the main molecular mechanisms of vascular calcification, and considers therapeutic strategies for vitamin К treatment.

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