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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We tested the hypothesis that a simple change in wall composition (medial calcium overload of elastic fibers) can decrease aortic elasticity. Calcium overload was produced by hypervitaminosis D plus nicotine (VDN) in the young rat. Two months later, measurement of central aortic mean blood pressure in the unanesthetized, unrestrained rat showed that the VDN rat suffered from isolated systolic hypertension but that mean blood pressure was normal. Wall thickness and internal diameter determined after in situ pressurized fixation were unchanged, as was calculated wall stress. Wall stiffness was estimated from (1) elastic modulus (determined with the Moens-Korteweg equation and values for aortic pulse wave velocity in the unanesthetized, unrestrained rat and arterial dimensions) and (2) isobaric elasticity (= slope relating pulse wave velocity to mean intraluminal pressure in the phenylephrine-infused, pithed rat preparation). Both increased after VDN, and both were significantly correlated to the wall content of calcium and the elastin-specific amino acids desmosine and isodesmosine. Left ventricular hypertrophy occurred in the VDN model, and left ventricular mass was related to isobaric elasticity. In conclusion, elastocalcinosis induces destruction of elastic fibers, which leads to arterial stiffness, and the latter may be involved in the development of left ventricular hypertrophy in a normotensive model.
Hypertension 1997 Apr
PMID:Calcification of medial elastic fibers and aortic elasticity. 909 90

Chronic sustained hypertension leads to structural changes of the small and large arteries. These alterations consist of smooth-muscle hypertrophy, increased deposition of collagen, and "dilution" or destruction of elastin fibers. In addition, there may be no growth at all, but a "rearrangement" of vascular wall material termed "remodeling." These changes serve to increase wall thickness and the media-to-lumen ratio and to decrease the external and internal diameter of the vessel--all of which contribute to increased systemic vascular resistance by the small arteries and increased impedance by the larger arteries. It has been suggested that these structural changes are an adaptive effort by the vessel to maintain a constancy of wall tension, but the end result is detrimental in that the effect is a further increase in systemic vascular resistance and blood-flow impedance, which lead to left ventricular hypertrophy and its consequences. The stimuli for these changes are stretch stimuli, mediated through stretch receptors on the arterial wall, and trophic stimuli mediated at the tissue level through the action of angiotensin II, aldosterone, and catecholamines. Angiotensin-converting enzyme inhibitors, especially those with effective tissue penetration, are ideal drugs to reverse these structural changes ("reverse remodeling"), decrease the systemic vascular resistance, and increase the vascular compliance. These agents exert their effects through suppression, at the tissue level, of angiotensin II, aldosterone, catecholamines, endothelins (ET1, ET3), and transforming growth factor-beta1 (TGF-beta1) and through an increase in local levels of kinins, prostaglandins, and nitric oxide, which have antigrowth effects. Although this is a class effect, it appears to be stronger with those angiotensin-converting enzyme inhibitors providing the greatest tissue penetration.
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PMID:Vascular remodeling: the role of angiotensin-converting enzyme inhibitors. 948 9

Arterial hypertrophy in response to hypertension includes increases in the connective tissue proteins elastin and collagen. Regression of arterial hypertrophy depends not only on blood pressure normalization but also on the specific antihypertensive treatment. Consequently, each drug class may exert an influence on connective tissue proteins. We evaluated the arterial connective tissue response of 16-week-old spontaneously hypertensive rats (SHRs) to treatment with minoxidil, 120 mg/L, drinking water for 10 weeks. Despite a decrease in blood pressure, minoxidil had no effect on arterial weight or collagen content but increased elastin content in the abdominal aorta, renal, and superior mesenteric arteries. The increase in elastin content in the abdominal aorta and superior mesenteric artery was accompanied by a decrease in tissue elastase activity. Thus the minoxidil-induced increase in arterial elastin content may be related to a direct effect of the drug to decrease elastase activity in these tissues.
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PMID:Arterial vasodilation and vascular connective tissue changes in spontaneously hypertensive rats. 964 83

Recent studies have shown that large-artery wall remodeling per se does not reduce distensibility in hypertension, indicating qualitative or quantitative changes in arterial components. The aim of the study was to determine in 1-year-old spontaneously hypertensive rats (SHRs) the changes in the elastic properties of large arteries, as assessed by the incremental elastic modulus (E(inc)), and the changes in the extracellular matrix, including fibronectin (FN) and alpha5beta1-integrin. The relationship between E(inc) and circumferential wall stress was calculated from in vivo pulsatile changes in blood pressure and arterial diameter by using a high-resolution echo-tracking system at the site of the abdominal aorta and in vitro medial cross-sectional area. E(inc)-stress curves and FN and integrin alpha5-subunit contents were determined for each animal. Mean stress and E(inc) were higher in SHRs than in Wistar rats. However, in a common range of stress, E(inc)-stress curves for SHRs were superimposable on those for Wistar rats, indicating that wall materials in both strains have equivalent mechanical behavior. Immunohistochemistry indicated that total FN, EIIIA FN isoform, and alpha5-integrin increased in the SHRs aortas without changes in elastin and collagen densities. Total FN was also increased in SHRs as determined by Western blot analysis. No differences in FN and alpha5-subunit mRNAs were detected between SHRs and Wistar rats. These results indicate that the aortic wall material of SHRs and Wistar rats have equivalent mechanical properties, although in SHRs it is subjected to a higher level of stress. By increasing cell-matrix attachment sites, FN may participate in the mechanical adaptation of both cellular and matrix components in SHRs.
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PMID:Fibronectin expression and aortic wall elastic modulus in spontaneously hypertensive rats. 967 62

We have recently demonstrated that in large arteries of spontaneously hypertensive rats (SHR), there is no increase of stiffness despite the increase in wall thickness, a sign of mechanical adaptation of the arterial wall to the higher level of stress. Because the dense plaques of smooth muscle are a major site of anchorage between the muscle cells and extracellular matrix, we determined by electron microscopy the distribution of dense plaques and their connections to elastic lamellae in the abdominal aorta of 1-year-old SHR and control Wistar rats. In vivo echo-tracking measurement of aortic distensibility and elastic modulus indicates a reduction of arterial stiffness in SHR compared with Wistar rats when they are studied over a common range of blood pressure. The media thickness to body weight ratio was higher in SHR than in Wistar rats. In the media, the percentage of sectional area occupied by extracellular matrix was not different between Wistar rats and SHR. The average number of dense plaques per muscle cell was not different between Wistar rats and SHR. However, the percentage of cell surface occupied by dense plaques was increased in SHR, and the percentage of cell surface connected to the elastic lamellae was twice as high in SHR compared with Wistar rats (9.4+/-1.5% versus 3.8+/-1.1%). These results suggest that the elastin network plays a major role in the mechanical adaptation of the arterial wall in SHR, not through variations of its total amount but through variations of the extent of anchorage to the muscle cells.
Hypertension 1998 Jul
PMID:Connection of smooth muscle cells to elastic lamellae in aorta of spontaneously hypertensive rats. 967 55

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

Heart disease remains the most frequent cause of death in the general population and is intimately related to aging. Either extreme premature aging or marked longevity may be monogenic, but in most humans aging is a complex polygenic phenomenon. Hypercholesterolemia and hypertension are important factors. Cardiac amyloidosis and vascular elastin degradation may be separate factors. Humans with the greatest longevity are relatively refractory to atherosclerosis. Frequencies of heart deaths among relatives of a heart-death proband without dyslipoproteinemia conform to expectations of a polygenic trait. Careful, attentive medical management of major environmental factors and of heart senescence can result in more successful aging.
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PMID:Genetics, aging, and the heart. 977 Sep 46

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

Mechanical properties of arteries are altered in some rat models of hypertension, and this may influence peripheral resistance and blood pressure as well as some of the complications of hypertension. It has usually been assumed that arterial wall stiffness is increased in hypertension, although recent studies suggest that this may not necessarily be the case in large arteries. We determined whether the mechanics of human resistance arteries are altered in hypertension. Subcutaneous resistance arteries (lumen diameter<300 microm) were isolated from hypertensive and normotensive subjects of similar ages (46+/-3 and 43+/-4 years, respectively). Vessels were mounted in a pressurized myograph, deactivated, and exposed to intraluminal pressures ranging from 3 to 140 mm Hg. At each pressure, lumen and media dimensions were measured. Media-to-lumen ratio and media width were greater in hypertensive vessels, reducing wall stress (P<0.01), whereas media cross section was similar in vessels from both groups. Isobaric elastic modulus (which is influenced by vessel geometry and by wall component stiffness) was lower in hypertensive vessels (P<0. 01). Stiffness of wall components (slope of incremental elastic modulus versus stress, which is geometry-independent) was significantly lower in hypertensive vessels (8.2+/-0.7) versus normotensive vessels (11.0+/-1.0, P<0.05), whereas distensibility was unchanged. Electron microscopic analysis of the media of the small arteries showed a greater collagen to elastin ratio (P<0.05) in the media of vessels from hypertensive patients. In conclusion, the stiffness of wall components (slope of elastic modulus versus stress) is not increased but is in fact decreased in subcutaneous resistance arteries from patients with mild essential hypertension. Reduced stiffness of resistance arteries from hypertensive patients does not appear to relate to changes in volume density of extracellular matrix components but may be the result of changes in extracellular matrix architecture or cell-matrix attachment, which remains to be established.
Hypertension 1999 Jan
PMID:Mechanics and composition of human subcutaneous resistance arteries in essential hypertension. 993 Nov 67


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