Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the processes controlling the accumulation of collagen and elastin in main pulmonary arteries of rats during an episode of hypoxic pulmonary hypertension. Explant cultures of main pulmonary arteries were incubated with [3H]proline to measure collagen and protein synthesis and percent collagen synthesis. Elastin synthesis was measured by [14C]valine incorporation into insoluble elastin. Relative collagen synthesis increased twofold (from 1.1 +/- 0.2 x 10(3) to 2.0 +/- 1.0 x 10(3) disintegrations per minute [14C]hydroxyproline/vessel/hr/mg protein), relative collagen synthesis doubled (from 2% to 4-5% of total protein synthesis), and elastin synthesis increased ninefold (from 0.4 +/- 0.2 x 10(4) to 3.6 +/- 0.6 x 10(4) dpm [14C]valine/vessel/hr/mg protein) in early hypertension. The level of pro alpha l(I) collagen RNA paralleled the relative collagen synthetic rate during the study period. Within 7 days of recovery from hypoxia, collagen and elastin contents were normal. We conclude that collagen and elastin in main pulmonary arteries are synthesized rapidly during an episode of hypoxic pulmonary hypertension and that collagen and elastin are rapidly removed from the hypertensive vessel during normoxic recovery.
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PMID:Collagen and elastin metabolism in hypertensive pulmonary arteries of rats. 231 97

Elastin of the ascending aortic media of 10 cases with type A dissecting aneurysm, 14 hypertensive cases, and 30 control cases were prepared by the treatment of aortas with hot formic acid, and three-dimensional architecture was observed by scanning electron microscopy. In the control cases, elastin showed framework-like continuous structure consisting of elastic laminae, and interlaminar fibers that interconnected the laminae. In 6 of 10 cases of dissecting aneurysm, the interlaminar fibers were apparently irregular in arrangement and shape, and decreased in number, especially in the outer media. This architectural alteration resulted in a rarefaction of interconnection between the elastic laminae in the media, and possibly resulted in the local weakness against the dissecting force of the laminae. This medial weakness may be related to the mechanism of initiation and progression of dissecting aneurysm. The cystic medial necrosis (CMN) was found in 3 cases, but only 1 of them was accompanied by a mild decrease of the interlaminar fibers in the area outside of CMN, suggesting that the initiation of CMN did not directly relate to the decrease of the interlaminar fibers. The aortic media of hypertensives generally showed an increase of interlaminar fibers, but their focal decrease was encountered in the outer media of 3 cases. These findings suggest that the decrease of the interlaminar fibers of medial elastin seen in dissecting aneurysms were related to hypertension.
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PMID:Alterations of elastic architecture in human aortic dissecting aneurysm. 235 59

The effects of hypertension and its treatment on the function and structure of arteries have been extensively studied, but no data are yet available on the effect of hypotensive drugs on the large arteries in normotensive rats. Two groups of 11-month-old normotensive breeder male rats were treated for 5 months, one with an angiotensin converting enzyme (ACE) inhibitor (MK-421, 2 mg/kg per day; n = 10) and the other with dihydralazine (15 mg/kg per day; n = 8). A group of 14 rats served as controls. Blood pressure was recorded every 14 days by the tail-cuff method. At the end of the treatment period (5 months), the rats were killed under anaesthesia and the descending thoracic aorta was removed and fixed. The different components of the aorta were assessed by automated morphometric image analysis after specific coloration of elastin (orceine), collagen (sirius red) and nuclei (haematoxylin after periodic acid oxidation. Both the ACE inhibitor and dihydralazine caused similar decreases in systolic blood pressure (SBP) compared with controls. This hypotensive effect was associated with a reduction in medial thickness, from 120 +/- 15 microns in controls to 104 +/- 9 microns in ACE inhibitor-treated and 103 +/- 10 microns in dihydralazine-treated normotensive rats. Elastin density significantly increased in the two treatment groups but the greatest increase was in the dihydralazine-treated group (P less than 0.001). Elastin fibre thickness increased significantly in the dihydralazine-treated group only. Collagen density was not significantly modified by either treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of vasodilatators on the structure of the aorta in normotensive ageing rats. 283 73

Abnormal accumulation of connective tissue in blood vessels contributes to alterations in vascular physiology associated with disease states such as hypertension and atherosclerosis. Elastin synthesis was studied in blood vessels from newborn calves with severe pulmonary hypertension induced by alveolar hypoxia in order to investigate the cellular stimuli that elicit changes in pulmonary arterial connective tissue production. A two- to fourfold increase in elastin production was observed in pulmonary artery tissue and medial smooth muscle cells from hypertensive calves. This stimulation of elastin production was accompanied by a corresponding increase in elastin messenger RNA consistent with regulation at the transcriptional level. Conditioned serum harvested from cultures of pulmonary artery smooth muscle cells isolated from hypertensive animals contained one or more low molecular weight elastogenic factors that stimulated the production of elastin in both fibroblasts and smooth muscle cells and altered the chemotactic responsiveness of fibroblasts to elastin peptides. These results suggest that connective tissue changes in the pulmonary vasculature in response to pulmonary hypertension are orchestrated by the medial smooth muscle cell through the generation of specific differentiation factors that alter both the secretory phenotype and responsive properties of surrounding cells.
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PMID:Smooth muscle-mediated connective tissue remodeling in pulmonary hypertension. 360 30

Hypertension results in increased thickness and stiffness of large artery walls. The goal of our study was to assess the respective roles of humoral factors such as Ang II, endothelin and blood pressure in these aortic modifications. For this purpose, uninephrectomized rats received DOCA and high salt diet, and when hypertension was installed, they were treated for 5 weeks with either a long-acting calcium antagonist, mibefradil (30 mg/kg/day), an ACE inhibitor, enalapril (3 mg/kg/day), or a mixed ETA and ETB endothelin receptor antagonist, bosentan (100 mg/kg/day). A group of hypertensive rats was left untreated and a sham-operated group of normotensive rats was used for control. At the end of treatment, aortic medial thickness and elastin as well as collagen were evaluated by quantitative morphometry. DOCA-salt hypertensive rats exhibited a marked increase in medial thickness associated with no change in absolute content in extracellular matrix. Elastin relative density decreased in DOCA rats. Enalapril had no effect on arterial pressure. Bosentan decreased slightly (by 12 mm Hg), but not significantly, blood pressure. None of these drugs had an effect on medial thickness suggesting that in DOCA hypertensive rats neither Ang II nor endothelin play a significant role in the remodeling of the aorta. In contrast, mibefradil almost normalized arterial pressure, prevented medial hypertrophy and increased elastin density. Further studies are required in order to assess if this effect is directly linked to the blood pressure decrease or to another mechanism related to the calcium antagonistic property of mibefradil.
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PMID:Respective role of humoral factors and blood pressure in aortic remodeling of DOCA hypertensive rats. 923 40

The structure of medial elastin determines arterial function and affects wall mechanical properties. The aim of this study was to (1) characterize the structure of elastin in terms of textural features, (2) relate structural parameters to total number of cardiac cycles (TC), and (3) determine the contribution of medial elastin to lumen mechanical stress. Images of pressure-fixed aortic sections stained for elastin were obtained from specimens collected postmortem from 35 animals of different species with a wide range of age, heart rate, and TC and divided into 2 groups: TClow=3.69+/-0.38x10(8) (n=17) and TChigh=15.8+/-2.38x10(8) (n=18) (P<0.001). A directional fractal curve was generated for each image, and image texture was characterized by directional fractal curve parameters. Elastin volume fraction and interlamellar distance were obtained by image analysis. Wall stress distribution was determined from a finite element model of the arterial wall with multiple layers simulating elastin lamellae. DFC amplitude was related to elastin volume fraction. Increased TC (TClow versus TChigh) was associated with lower directional fractal curve amplitude (0.23+/-0.02 versus 0.14+/-0.02; P<0.001), reduced elastin volume fraction (36.5+2.6% versus 25.7+2.1%; P<0.01), and increased interlamellar distance (8.5+/-0.5 versus 11.5+/-1.0 microm; P<0.05). Loss of medial elastic function increased pressure-dependent maximal circumferential stress. Structural alterations of medial elastin, quantified by fractal parameters, are associated with cumulative effects of repeated pulsations due to the combined contribution of age and heart rate. Loss of medial functional elasticity increases luminal wall stress, increasing the possibility of endothelial damage and predisposition to atherosclerosis.
Hypertension 1998 Jul
PMID:Quantification of alterations in structure and function of elastin in the arterial media. 967 56

To examine arterial mechanical changes during aging, pressure-radius and axial force-radius curves were measured in vivo in carotid arteries from 6- and 23-month-old Brown Norway X Fischer 344 rats. Incremental passive circumferential stiffness (measured at 50, 100, and 200 mm Hg) was higher (P<0.01) in the 23- compared with the 6-month-old rats (14.02+/-1.23 versus 6.58+/-1.51; 2.68+/-0.56 versus 0.99+/-0.34; 1.10+/-0.24 versus 0.69+/-0.15 dyne/mm2x10(3), respectively). Incremental passive axial stiffness was increased (P<0.01) in the 23- compared with the 6-month-old rats (7.95+/-0.70 versus 4.24+/-0.81; 1.91+/-0.10 versus 0.61+/-0.16; 0.58+/-0.09 versus 0.36+/-0.06 dyne/mm2x10(3), respectively). Active incremental circumferential arterial stiffness at 100 and 200 mm Hg was increased (P<0.01) in the older rats. In 6-month-old rats, activation of vascular smooth muscle enhanced (P<0.01) the incremental circumferential and axial stiffness measured at 200 mm Hg. In 23-month-old rats, only active incremental stiffness was increased (P<0.01) at 200 mm Hg. Aging increased (P<0.05) media thickness, collagen content, and the collagen/elastin ratio by 12%, 21%, and 38%, respectively. Elastin density and the number of smooth muscle cell nuclei were decreased by 20% and 31%, respectively, with aging. Thus, structural alterations that occur with aging are associated with changes in both active and passive stiffness. Vascular smooth muscle tone modulates arterial wall anisotropy differently during aging.
Hypertension 1998 Sep
PMID:Large artery remodeling during aging: biaxial passive and active stiffness. 974 Jun 8

Edema, proteinuria, hypertension (EPH) gestosis is accompanied by an increase of collagen content and premature replacement of hyaluronic acid by sulfated glycosaminoglycans both in the umbilical cord arteries and in Wharton's jelly. The effect of EPH gestosis on elastin content and metabolism in the umbilical cord arterial wall was the aim of this work. Studies were performed on normal umbilical cord arteries and those taken from newborns of mothers with EPH gestosis. Elastin was isolated from the arterial wall and quantified by a dye-binding method. Biosynthesis and degradation of this protein was evaluated by a pulse-chase experiment with the use of 14C-proline. It was found that EPH gestosis is associated with a significant reduction of elastin content in the umbilical cord arteries as a result of decrease in elastin biosynthesis rate and accelerated degradation of this protein. The replacement of elastin by collagen, and hyaluronate by sulfated glycosaminoglycans, may decrease the hydration of arterial wall and reduce its elasticity. Such rearrangement of extracellular matrix of the umbilical cord arteries may affect mechanical properties of these vessels and disturb fetal blood circulation.
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PMID:Elastin of the umbilical cord arteries and its alterations in EPH gestosis (preeclampsia). 985 59

Pre-eclampsia--edema, proteinuria, hypertension (EPH-gestosis) is one of the more common complications observed during pregnancy. The umbilical cord vein walls were taken from newborns delivered by healthy mothers (control material) and by mothers with polysymptomatic pre-eclampsia (investigated material). Normal saphenous vein walls were collected from adult subjects undergoing varicose vein surgery. The collagen content was measured by the assay of hydroxyproline. Elastin was determined according to Fastin Elastin Assay and gravimetrically. Glycosaminoglycans content was determined by uronic acids assay. The collagen content decreased in the pre-eclampsia material. The amount of soluble elastin increased in the investigated material. The insoluble elastin content decreased in the umbilical cord veins of newborns delivered by mothers with pre-eclampsia. Reconstructing the umbilical cord vein wall may disturb fetal blood flow and affect the vascular system in adulthood.
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PMID:Extracellular matrix components of the wall of umbilical cord vein and their alterations in pre-eclampsia. 1087

Our aim was to determine the structural factors that determine the mechanical adaptation of the carotid arterial wall in stroke-prone hypertensive rats (SHRSP). Distensibility-pressure and elastic modulus-stress curves assessed by in vivo echo-tracking measurements indicated a reduction in arterial stiffness in 13-week-old SHRSP compared with Wistar-Kyoto rats (WKY). Elastin and collagen contents determined biochemically were not different between SHRSP and WKY. Confocal microscopy showed that the mean area of fenestrations and fraction of area occupied by fenestrations of the internal elastic lamina (IEL) were smaller in SHRSP than in WKY, which indicated a reduction in stress-concentration effects within the IEL. Immunohistologic staining of EIIIA fibronectin isoform and total fibronectin (also as determined by Western blot) was greater in SHRSP, which suggested increased cell-matrix interactions. We suggest that these structural modifications of the vascular wall play a synergistic role in the mechanical adaptation to a high level of stress in SHRSP.
Hypertension 2001 Apr
PMID:Fenestrations of the carotid internal elastic lamina and structural adaptation in stroke-prone spontaneously hypertensive rats. 1130 10


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