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

Broad-breasted white male turkeys develop hypertension, tachycardia and aortic arteriosclerosis spontaneously by approximately 5 weeks of age. When fed B-aminopropionitrile (BAPN), aortic tensile strengths are lowered, and a high percentage of the turkeys die from aortic dissecting aneurysms. There are essentially no deaths from aneurysms when either dl-propranolol or reserpine is fed in concert with BAPN; practolol and soltalol partially protect the BAPN-fed turkey from lethal aneurysms while hydralazine and phenelzine sulphate potentiate mortality from aneurysms. Dl-propranolol decreases and reserpine increases dP/dtmax and both drugs lower arterial pressure and heart rate when fed with BAPN. Such diets also decrease the ultrastructural disarray of collagenous and elastic fibres in the media of the abdominal aorta that occurs from the feeding of BAPN and thereby raise aortic tensile strength. Sotalol and practolol when fed to BAPN-fed turkeys lower blood pressure and dP/dtmax, but neither drug affects aortic tensile strength and both counteract the deleterious effect of BAPN on the ultrastructure of collagenous and elastic fibres to a minor degree. Phenelzine sulphate does not affect arterial pressure while hydralazine reduces arterial pressure; both drugs decrease aortic tensile strength and increase the ultrastructural disruption of aortic elastin and collagen in the BAPN turkey. The results suggest that dl-propranolol, reserpine, phenelzine sulphate, and hydralazine have an action on aortic tissue and indicate the usefulness of the BAPN-fed turkey as a model for identifying potential drug effects on aortic elastin and collagen.
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PMID:The B-aminopropionitrile-fed turkey: a model for detecting potential drug action on arterial tissue. 685 Jul 14

Segments of carotid and tail artery, and thoracic aorta from control and hypertensive animals (DOCA + salt) were used for the study of mechanics and/or chemical composition. Pressure-diameter measurements were made on intact segments under conditions of active (145 mM-K+) and passive (O-Ca++ and 2 mM-EGTA) smooth muscle. Segments were used for chemical analyses of connective tissue content, water spaces, and electrolyte content. The passive stiffness of carotid and tail arteries increased monotonically with time. The carotids showed significant changes after two weeks of hypertension while the tail arteries only after 12 weeks. The collagen and total connective tissue content of the hypertensive arteries was decreased while collagen/elastin was unchanged. Smooth muscle activation produced larger changes in diameter of hypertensive arteries especially at higher values of transmural pressure. Maximum active force development was increased in carotid arteries at each time period from +2 weeks on while it was increased for the tail arteries only at +2 and +4 weeks. Relative cellular volume of these arteries was monotonically increased with hypertension. Maximum active force normalized to cellular content was not significantly different for carotid arteries from control and DOCA rats. For hypertensive tail arteries normalized on this basis force development remained elevated at +4 weeks but was significantly reduced at +12 weeks. Not all of the response to smooth muscle activation are monotonic with duration of hypertension, nor can all of these changes be explained on the basis of changes in cellular volume.
Hypertension
PMID:Time course of arterial wall changes with DOCA plus salt hypertension in the rat. 706 Nov 25

After unilateral nephrectomy and bilateral adrenal enucleation at 5 weeks of age, salt-loaded rats developed hypertension (ARH) at 6 weeks. Fibrous vascular protein and in vivo incorporation of 3H-lysine into this protein fraction were measured at 15 weeks of age in these animals. This study demonstrates: (1) that incorporation rates of 3H-lysine into cardiac collagen and elastin in ARH rats were greater than in control rats (p less than 0.001, respectively), and (2) that administration of phenoxy-benzamine hydrochloride decreased the incorporation of tritiated lysine into cardiac collagen in ARH rats, concomitant with a reduction in blood pressure. Based on these findings, increased synthesis of cardiac collagen and elastin appears to play an important role in the development of hypertension in ARH.
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PMID:Enhanced protein synthesis of heart in adrenal-regeneration hypertension and its reduction following antihypertensive treatment. 716 78

Carotid and tail arteries from 20-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were used to compare mechanics and biochemical properties. Measurements of pressure-diameter relations were made on isolated segments under conditions of active (145 mM K+) and passive (O mM Ca+2 and 2 mM EGTA) smooth muscle. Connective tissue, water and electrolyte contents, and extracellular water spaces were determined. Chemical data were also obtained from segments of thoracic aorta. The passive mechanics of arteries from the SHR were stiffer compared to those from WKY. Total connective tissue content (collagen + elastin) and collagen/elastin ratio were both smaller in the SHR arteries. Differences in the characteristics of the connective tissue matrix other than total content must exist in SHR and WKY arteries. Maximum values of active stress (force/area) developed by SHR arteries were larger and occurred at smaller values of wall strain compared to WKY arteries. The maximum reduction in wall diameter with smooth muscle activation was larger in the WKY arteries, but these constriction responses were better maintained at higher pressures by SHR arteries. Extracellular water space was lower in SHR arteries, while total water content was not different. The fraction of the wall of SHR arteries occupied by smooth muscle cells was larger than that of WKY arteries. When values of maximum active stress were normalized to the relative cell content, no difference was found for SHR and WKY carotids, but SHR tail arteries still produced a significantly larger active cell stress than WKY tail arteries. This suggests that intrinsic differences exist in the properties of smooth muscle cells of SHR and WKY tail arteries.
Hypertension
PMID:Basis for the altered arterial wall mechanics in the spontaneously hypertensive rat. 730 10

A combined transmission (TEM) and scanning (SEM) electron microscopic study was performed on aortae of deoxycorticosterone-salt (DOC-salt)-treated rats and spontaneously hypertensive rats (SHR) to compare the effects of hypertension as well as its reversal on the aortic intima. To best reproduce the in vivo state of the vasculature, rats were perfusion-fixed at pressures corrected for each individual animal (30 mm Hg below measured systolic pressure). The intimal alterations were focal and thus were best appreciated with the combined use of SEM and TEM. Qualitatively, both models of hypertension showed similar intimal changes, which consisted of subintimal thickening due to an accumulation of both extracellular material and cells. Subendothelial cells with a morphology indicating a blood-borne origin were present simultaneously with cells derived from the vessel wall. The increased subendothelial extracellular material included precipitated plasma proteins, reticulated basement membrane, collagen fibers, and fragments of elastin. Increase in the height of endothelial cells with distortion of nuclear shape was prominent. Withdrawal of DOC-salt combined with low-salt diet for 11 weeks did not result in a discernible regression of these intimal changes despite normalization of blood pressure. We conclude that vascular injury, once induced, may be difficult to reverse and suggest that areas of prior damage may serve as foci for later vascular complications.
Hypertension
PMID:Effects of hypertension and its reversal on aortic intima lesions of the rat. 737 54

Vessels of known position in the vascular tree of the kidneys of two cases with a long history of progressive systemic sclerosis--one normotensive, one hypertensive--were examined morphometrically. Medial thickness, intimal thickness and the relative content of collagen and elastin in the vascular media were measured. Smooth muscle nuclei were counted in the arterial cross section. These morphometric data were compared with those obtained from two autopsy cases--one with a history of essential hypertension, one without any hypertensive history. The findings suggest that progressive sclerosis induces intimal thickening in all branches of the renal artery down to a distented diameter of 200 microns. In the case where progressive sclerosis was complicated by arterial hypertension increased medial thicknesses were found, similar to the findings in the case with a history of essential hypertension.
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PMID:Morphometry of intrarenal arteries in progressive sclerosis. 741 45

Clear evidence has not yet come concerning the genetics of abdominal aortic aneurysms (AAA). There are circumstantial proof for a hereditary predisposition. In a retrospective study of sixty patients consecutively underwent a surgical repair for AAA, showed that one third of them knew a first-degree relative with the same disease. Environmental factors, such as smoking, ageing or hypertension, must be taken into account. A multifactorial mode of inheritance is under discussion due to both multiple genes with different expressivity and diverse environmental factors. Linkage-analysis or DNA sequencing of the different gene loci in population studies or sibbling-analysis are the tools in search for candidate genes for inheritance of AAA. Mutations in those genes encoding structural components of the aortic wall, such as collagen-type-III, fibrillin or elastin, are not taken to be the underligned genetic cause. Mutations in genes encoding enzymes for the turnover of the aortic wall components, such as alpha-1-antitrypsin or matrix-metalloproteinase-2, may play an important role.
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PMID:[Mode of genetic inheritance of abdominal aortic aneurysm: still no clear answers]. 758 55

In large arteries the structure of the arterial wall determines pulsatile hemodynamics of pressure and flow. Mechanical wall stiffness, wall thickness, and elastin and collagen content vary along the arterial tree. The contribution of genetic and environmental factors to such structural properties is not yet known, but some data are available on possible functional correlates. In hypertensive rats diastolic and pulse pressure have been shown to be linked to two different genes on separate chromosomes. Although a genetic component contributes to intimal calcification, medial hypertrophy is not associated with genetic factors. A study of French West Indies families showed a preferential genetic determinant for pulse pressure in contrast to systolic or diastolic pressure. Environmental and geographic factors are associated with markedly different prevalences of hypertension and age-related increases in arterial stiffening in urban and rural communities in China. Salt consumption has also been implicated in modifications of pulse wave velocity. Recent data on structural parameters of the aortic trunk in oriental (Chinese) and occidental (American and Australian) subjects have shown that the ascending aorta in oriental subjects is of a relatively large diameter and thinner media. This suggests that in this population a relatively higher primary pressure pulse would be generated because of increased stiffness of the proximal aorta. This suggests that factors other than arterial pressure are responsible for structural differences in the aortic wall and that oriental populations may have a predisposition to increased arterial pressure based on structural factors that affect the interaction between ventricular ejection and arterial load.
Hypertension 1995 Jul
PMID:Genetic and environmental factors in the function and structure of the arterial wall. 760 29

Structural changes of the peripheral vascular component as seen during hypertension and atherosclerosis have been suggested during heart failure but have never been reported. Therefore, we studied possible structural alterations in the peripheral vasculature in an experimental model of heart failure, induced by ligation of the left coronary artery in rats. Large conduit and resistance-type arteries were excised at 1, 3, 5, and 12 weeks after myocardial infarct induction (MI) or sham surgery. Vessel dimensions (medial cross-sectional area [CSA], internal and external diameters, and media-to-lumen ratios) as well as medial collagen and elastin volume fractions were measured by computerized morphometry. The hydroxyproline assay was used to determine collagen and elastin content biochemically. In separate groups of animals, peripheral tissue flows were measured by using radioactive microspheres 5 and 12 weeks after MI. To evaluate the effects of the degree of heart failure, the animals of the 12-week group (n = 10) were subdivided into groups of moderate (< 45% infarct size) and large (> 45% infarct size) infarction. At all time points, body weights of sham-operated and MI rats were comparable. Lung weights of infarcted animals were increased proportionally to infarct size. No major changes in vessel dimensions were seen at the earlier time points. Twelve weeks after coronary artery ligation, significantly smaller CSAs were observed in several large conduit arteries such as the thoracic aorta, carotid artery, and superior mesenteric artery. These changes coincided with reductions in both internal and external diameters. In contrast, internal and external diameters of mesenteric and pulmonary resistance arteries were increased after 12 weeks of coronary artery ligation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peripheral vascular alterations during experimental heart failure in the rat. Do they exist? 767 Sep 66

The pathogenesis of abdominal aortic aneurysm involves many factors acting over time. However, destruction of elastin in the aortic wall is a key event that shifts the load produced by blood pressure on to collagen. This is exacerbated in the presence of hypertension. Smoking and age are further important factors, as is the site; elastic lamellae are relatively less common in the abdominal aorta. Once the shielding effect of elastin is lost, further dilatation and rupture of the aorta depend on the physical properties of the collagen present.
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PMID:Pathogenesis of abdominal aortic aneurysm. 792 83


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