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

The contribution of drinking fluid salt to the development of deoxycorticosterone (DOCA) hypertension and arterial wall changes was assessed in unilaterally nephrectomized rats. Half of the DOCA-treated animals received saline supplemented with 0.2% KCl and the other half received deionized water as drinking fluid. All animals were fed standard rat chow (Na content = 0.36%). After 8 weeks, arterial pressures were significantly elevated in both DOCA groups to values which were not significantly different. The heart weight to body weight ratio was also elevated in both DOCA groups with a larger response in the saline-treated ones. Body weight of saline-treated DOCA rats was significantly lower than untreated controls and water-treated DOCA rats. Arteries from both DOCA groups exhibited increased passive stiffness, larger maximum active stress, wall thickening, decreased collagen and elastin concentration, greater relative cell volume, and greater water and cation concentrations. Larger changes were generally found in the saline- than the water-treated group. These results show that saline administration is not necessary for the development of hypertension or hypertension-induced arterial wall changes in DOCA-treated, uninephrectomized rats. Hypertension developed more slowly and arterial wall changes were similar in magnitude in water-treated animals. These results suggest that the rate and/or time history of pressure elevation may be an important factor contributing to hypertension-related arterial changes.
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PMID:Contribution of salt to arterial wall changes in DOCA hypertension in the rat. 342 65

As a result of aging, a variety of structural and biochemical changes occur in arterial walls that result in hemodynamic adaptations. With age, there is a thickening of intima and media, together with an increase in the number of smooth muscle cells, synthesis of collagen and elastin, and deposition of calcium, glycosaminoglycans, free and esterified cholesterol, and sphingolipids. These changes are similar to those observed in atherosclerosis, which is accompanied by marked increases of intimal smooth muscle cells and connective tissue constituents. The net effects of both aging and atherosclerosis are a loss of elasticity and distensibility. This results in a decrease in arterial compliance or capacitance, which in turn means that with increasing age systolic blood pressure (SBP) tends to be higher, and diastolic blood pressure (DBP) lower. As a consequence of structural changes both in myocardium and vessels, cardiac output and renal and hepatic blood flow undergo adaptive alterations in order to meet the requirements of central hemodynamics and peripheral circulation. The implications of these processes of aging demand appropriate treatment of cardiovascular disorders, in particular hypertension, which occurs in 30-50% of patients above the age of 60 years. Appropriate treatment may demand dose adjustment and careful selection of antihypertensive drugs with a minimum of side effects, which additionally are capable of diminishing preload and afterload.
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PMID:Aging and the cardiovascular system. 344 May 23

Malignant renal hypertension was induced in male Wistar rats. In the early phase of the disease, ie. the 1st week, a transient and generalized activation of arterial cellular functions was observed, while later, on day 21 widespread intimal proliferations developed in the arteries. This early activation included an increase in transmural permeability, DNA-, protein, collagen, elastin and ground substance synthesis, a rise in mural PGI2 content and an increase in number of Weibel-Palade bodies. An activation of platelets and monocytes could also be detected during the 1st week. In a group of rats the development of malignant hypertension was interrupted following the early activation of arteries and the incidence of intimal proliferations was compared with that of rats with maintained hypertension. No intimal proliferation was observed on day 21 in the rats with interrupted hypertension. It is concluded that the early activation of the artery does not furnish enough stimulus for triggering intimal proliferations and intimal plaques are not direct sequelae of the early arterial reaction. Furthermore the entrance of plasma materials during transmural permeability increase can not induce smooth muscle proliferation if the hypertension is interrupted.
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PMID:Relationship between the early arterial reaction to hypertension and the development of intimal proliferation. 351 39

The events involved in atherogenesis include platelet deposition on damaged endothelial surfaces; migration and proliferation of smooth muscle cells; the formation of elastin, collagen, and glycosaminoglycans, followed by the penetration and complexing of lipoproteins; and, calcification. Since calcium is involved in these and other events, considerable data exist on the effects of altering calcium influx in experimental atherosclerosis. Interventions that increase calcium deposition tend to increase the severity of experimental atherosclerosis, whereas interventions that reduce calcium entry into cells tend to reduce its progression. Using rabbits, researchers have recently focused on the ability of calcium channel blockers, such as nifedipine, verapamil, and diltiazem, to attenuate the development of experimental atherosclerosis. Studies also suggest that although calcium channel blockers may protect against the development of experimental atherosclerosis, they are less effective in inducing its regression. Further, studies with calcium channel blockers in rabbits deficient in low-density lipoprotein receptors did not show protection against the development of atherosclerosis. However, no clinical studies are yet available to judge the potential protective effects of calcium channel blockers in humans. Since many patients are now receiving long-term calcium blocker therapy for hypertension, these findings may be relevant in the selection of antihypertensive therapy, provided that protective effects can be demonstrated.
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PMID:Calcium channel blockers and atherogenesis. 355 1

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

In order to study the role of elastin in arteries with respect to hypertension and hypertensive arterial disease, aortic elastin content and elastase-like enzyme activity were examined and compared in stroke-prone spontaneously hypertensive rats (SHRSP), which show malignant hypertension, and Wistar-Kyoto normotensive rats (WKY). The elastin content was lower, whereas the elastase-like activity was higher at 20 weeks of age in SHRSP than in WKY, so that the aortic elastin/enzyme ratio of SHRSP was lower than that in WKY. These differences were not found at 6 weeks of age (prehypertensive stage). For SHRSP anti-hypertensive treatment resulted in lowering the elastase-like activity and in increasing the elastin content in comparison to untreated animals. The subcellular distribution of the elastase-like activity closely correlated with that of 5'-nucleotidase activity, a plasma membrane marker enzyme. The results indicate involvement of a smooth muscle plasmalemmal elastase-like enzyme in vascular connective tissue metabolism in health and possibly also its participation in hypertensive arterial diseases.
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PMID:Elastin and elastase-like enzyme change in aorta of rat with malignant hypertension. 364 94

The biosynthesis of collagen and elastin was followed during the development of spontaneous hypertension in rats (SHR) of the Okamoto-Aoki strain. Strain-matched animals of the same age, which did not develop hypertension, served as controls. Both collagen and elastin synthesis (as revealed by specific hydroxyproline activity) was found to exceed control levels in the prehypertensive period, to decrease during the development of hypertension and to increase again in the period of the established hypertensive state. From the two main collagen types present, synthesis of collagen type III exceeded that of type I in the prehypertensive period (at the age of 4 weeks) and this relation was reversed during the period of established hypertension. It is suggested that (a) the vascular connective tissue metabolism in SHR differs from that in strain-matched controls, and (b) the reverse rate of collagen type III to collagen type I synthesis during hypertension development may be considered an adaptive response to the increasing pressure load which may alter the mechanical properties of the vessel wall.
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PMID:Collagen and elastin synthesis in the aorta of spontaneously hypertensive rats. 365 20

The collagen and elastin contents of the major arterial components of the canine circle of Willis (basilar artery, posterior cerebral artery, internal carotid artery, middle cerebral artery, and anterior cerebral artery) were determined as measures of the passive mechanical properties of these vessels. Studies were carried out in seven normotensive dogs and seven dogs in which experimental renal hypertension of 3 months duration had been induced. In the normotensive animals, the collagen content of the middle cerebral artery exceeded that of the other vessels considered. The elastin content and the total connective tissue were not significantly affected by arterial site. The middle cerebral artery collagen to elastin ratio was greater than corresponding values for the basilar, posterior cerebral, and internal carotid arteries. Connective tissue differences were less pronounced in the hypertensive animals. No component of the canine circle of Willis in the hypertensive dogs showed a significantly different collagen content, elastin content, total connective tissue content, or collagen to elastin ratio. In comparing cerebral vessels from normotensive and hypertensive dogs, total connective tissue values were greater in hypertension for all arterial sites considered. These acute physiological changes in connective tissue content over small distances in intracranial blood vessels from normotensive animals, together with unique connective tissue responses of these vessels to short term hypertension, may suggest additional possible factors important in the natural history of cerebrovascular pathological conditions.
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PMID:Connective tissue analysis of the canine circle of Willis in hypertension. 369 97

The extracellular matrix of blood vessel walls contains elastin, collagen, and proteoglycans, all of which can affect vascular resistance and, hence, blood pressure by virtue of their biomechanical properties. In the present study, we have begun to explore the possibility that proteoglycans may play a role in the pathophysiology of hypertension by analyzing, qualitatively and quantitatively, the polysaccharide components of proteoglycans from aorta of two normotensive rat strains, Wistar Kyoto (WKY) and Wistar rats, and from spontaneously hypertensive (SH) rats of the Okamoto strain. The total concentration of aorta glycosaminoglycans in the SH rat was 33% higher than in the WKY rat, due to a 164% increase in chondroitin 4- and 6-sulfate. The content of dermatan sulfate (DS), hyaluronic acid (HA), and heparan sulfate (HS) was similar in the two strains. The 4-wk-old SH rat also had an increase in chondroitin sulfate (CS) compared to the 4-wk-old WKY rat, without any change in DS, HA, or HS. The Wistar rat had approximately the same concentration of CS und DS in the aorta as the WKY rat, but HS und HA were reduced by 62 and 37%, respectively. The galactosaminoglycans (CS and DS) were heterogeneous on cellulose acetate electrophoresis and exhibited a different pattern for each of the three strains. Undersulfated CS accounted for 15% of the total CS in WKY aorta but was present in only trace amounts in the SH aorta; 2% of the CS from the Wistar aorta was undersulfated. In all three strains, DS was exclusively 4-sulfated, and the CS contained approximately equal amounts of 4- and 6-sulfated galactosamine residues. Ultrastructural studies demonstrated that the HS was localized in the subendothelial matrix and the pericellular region surrounding the medial smooth muscle cells. CS and DS were primarily associated with collagen in the media. In the SH rat aorta the subendothelial matrix was thicker, and there was a relative increase in the CS/DS in the smooth muscle cell pericellular matrix. We suggest that, if similar alterations in CS proteoglycans are present in the resistance vessels, these changes may contribute to the increased peripheral vascular resistance in the hypertensive animal.
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PMID:Proteoglycans and hypertension. I. A biochemical and ultrastructural study of aorta glycosaminoglycans in spontaneously hypertensive rats. 372 Feb 75

This report describes an investigation of the effects of developing hypertension on the synthesis and accumulation of insoluble elastin in the thoracic aorta of young rats. Uninephrectomized male rats were made hypertensive by administration of deoxycorticosterone acetate and addition of 1% NaCl to their drinking water. Divergence of systolic blood pressures between treated and control animals and hypertrophy of the vessel began after about 2 weeks of treatment. Coincident with the appearance of hypertrophy, there was an increased accumulation of insoluble elastin in the aorta and a large increase in the capacity of the aortic tissue to synthesize elastin. However, in spite of continued increases in blood pressure and vessel hypertrophy, this effect on elastin synthesis and accumulation was transient. The results of this study suggest that synthesis of elastin in aortic tissue of young rats is highly sensitive to alterations in blood pressure.
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PMID:The effect of developing hypertension on the synthesis and accumulation of elastin in the aorta of the rat. 396 64


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