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

Thirty consecutive patients with severe scleritis or episcleritis were admitted as in-patients to the Medical Ophthalmology Unit and assessed for systemic disease. There were seventeen women and thirteen men. The mean age was 53 with a median of 57 (range 23-83). Eighteen of the patients had scleritis: eleven of these had evidence of connective tissue disease and three of them had temporal arteritis. Twelve patients had episcleritis: six of them had a collagen disease and one of them developed temporal arteritis. This high incidence of temporal arteritis in association with scleritis has not been previously reported. It is important to diagnose and treat overt temporal arteritis early with parenteral steroids so that ischaemic papillopathy can be avoided. A higher incidence of collagen diseases than previously described is reported in episcleritis. It is thought that this is secondary to selection since patients with the usual self-limiting episcleritis are not normally referred for further in-patient investigation. In no patient was more than one significant diagnosis made. There was no significant medical illness in only 11% of patients with scleritis and 33% of patients with episcleritis. The majority of the non-collagen diseases (e.g. hypertension) were not previously recognized. In none of the patients with temporal arteritis was the diagnosis made before admission. It is concluded that full examination and investigation for underlying disease is indicated in both scleritis and severe episcleritis.
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PMID:Scleritis and temporal arteritis. 101 96

The autopsy findings in a 2-year-old girl with severe hypertension resulting from stenosis of the lower part of the thoracic and the abdominal aorta were reviewed. The lower portion of the thoracic aorta and the abdominal aorta showed uniform narrowing down to the level of the bifurcation of iliac arteries. Histologically, the aortic wall of the stenotic site showed irregular proliferation of smooth muscle cells and collagen fibers. The elastic fibers had disappeared from outside the media. No intimal thickening and inflammatory cell infiltration were observed. These histologic changes of the aortic media in this case are apparently similar to fibromuscular dysplasia (medial hyperplasia).
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PMID:Tubular stenosis of the aorta with aortic fibromuscular dysplasia. 103 77

Evidence from actuarial statistics, epidemiologic studies, and laboratory experiments clearly indicates that hypertension has an accelerating effect on atherogenesis, and this atherogenesis appears to be a graded function of elevated intra-arterial pressure. The fact that atherosclerosis occurs preferentially in the abdominal aorta and iliofemoral arteries seems likely to result from the pressure augmentation by reflected pulse waves that is intensified by vasoconstriction and also by the increase in hydrostatis pressure that results from gravitational stress during standing. Vasoconstriction is a characteristic of hypertension and occurs also with upright posture. The predilection of the coronary epicardial vessels for atherosclerosis seems likely to relate to subtle pressure-volume changes in these arteries as a result of this vascular bed being in the highest pressure area of the arterial system and because intramyocardial arterial branches are completely occluded during systole. The possibility is presented that hypertension accelerates atherosclerosis because it is a metabolic determinant of the multifunctional arterial smooth muscle cells which have the potential for forming collagen and mucopolysaccharides as well as phospholipid.
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PMID:The relationship of hypertension to coronary, aortic, and iliofemoral atherosclerosis. 109 12

Temporary hypertensive increases in blood pressure, or variations in blood pressure when there was an already existing hypertension, in which the blood pressure either moved within the limits of hypertensive blood pressure values or temporarily returned to normal, occurred in 129 men ages 23-85, in whom repeated measurements of the blood pressure and pulse wave rate (PWG) were carried out in the aorta and iliac artery in the course of a longitudinal study over years. Both categories--temporary and chronic hypertensives--showed significant differences in the height of the PWG increase per 10 mm Hg (delta-c-p). The delta-c-p value for the chronic hypertensives (n equals 43) was 0.73 plus or minus 0.35 m/sec, that of the temporary hypertensives 0.56 plus or minus 0.24 m/sec (p smaller than or equal to 0.01). The mean value for both groups was 0.62 plus or minus 0.29 m/sec. Delta-c-p increased with age (0.54 m/sec yields 45th year; 0.60 m/sec from 46-55 years; 0.61 m/sec from 55-65 years; 0.67 m/sec at 66 and over). The increase of delta-c-p with age is caused by the increase in chronic hypertension. Delta-c-p was constant over a mean pressure range of 90-190 mm Hg in temporary and chronic hypertensives, irrespective of the amount of the (individual) mean difference in pressure, but it was distinctly greater in chronic than in temporary hypertensives. On lowering pressure, the delta-c-p was also greater in chronic than in temporary hypertensives. When normal pressures were attained, temporary hypertensives showed no differences from the PWG of normotensive of the same age. The differences between temporary and chronic hypertensives are explained by the different relations in the structure of the wall of the aorta, but especially because the function of the muscular layer was better maintained in temporary hypertensives. The raising of the PWG in temporary hypertensives is probably caused by the increased tension in the wall alone. Whether, in addition to the increased incorporation of collagen and a rarification of the smooth muscle, the thickness to radius ratio also increases above that usual for the age group in chronic hypertension is still not clear, but it is not essential for the explanation of the greater increase in the delta-c-p. The longitudinal delta-c-p values obtained in individual subjects confirms the transverse delta-c-p findings, with regard to size and age group, which were obtained by comparisation of cross sections of groups of normotive and hypertensive subjects.
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PMID:[A longitudinal study of the relationship between the pulse wave velocity in the aorta-iliaca vessel and the blood pressure (author's transl)]. 112 18

The selectively-bred substrains of spontaneously hypertensive rats with a greater vulnerability to vascular lesions rapidly developed arterial fat deposition within 1 or 2 weeks as well as a greater hypercholesterolemic response when fed on high fat cholesterol diet including 20% of suet, 5% of cholesterol and 2% of cholic acid. The ring-like arterial fat deposition at the branches of superior mesenteric arteries and cerebrobasal arteries, which was found to be good indices for the deposition of intrarenal or coronary arteries, was not observed in normotensive rats fed on high fat cholesterol diet for 3 months, greatly delayed in SHR under antihypertensive treatment and accelerated by 1% salt loading in drinking water. The horseradish peroxidase infused intravenously 1 to 4 hours before sacrifice leaked in ring-like forms which corresponded to the fat deposit in mesenteric arteries. The incorporation of 3H-proline infused 4 hours before sacrifice was enhanced in the mesenteric arteries with the fat deposition. These results clearly indicated that hypertension was a great contributory factor to rapid arterial fat deposition, which was caused by an increased vascular permeability and enhanced the arterial collagen formation, the initiation process of arterio- or atherosclerosis.
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PMID:Pathogenesis of acute arterial fat deposition in spontaneously hypertensive rats. 115 92

Biphasic collagen-induced platelet aggregation, resembling that induced by epinephrine, was noted in platelet-rich plasma (PRP) of 11 stroke and 1 coronary disease patients. Similar pattern of aggregation was not observed in normal PRP. The occurrence of the biphasic collagen aggregation does not appear to relate to platelet count, smoking habit, medication, or other abnormalities such as hypertension, diabetes, and elevated serum lipid levels. However, platelets of these patients were very sensitive to aggregating agents including epinephrine and adenosine diphosphate. The concentration of collagen that elicited biphasic aggregation in these platelets was too weak to aggregate platelets of normal subjects. We believe that the release threshold of these platelets is reduced to such an extent that minute amounts of collagen, which would be insufficient to induce release from normal platelets, are capable of inducing release from these platelets. Both phases of collagen induced aggregation are probably resulted from the activation of the release mechanism.
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PMID:Characterization and significance of collagen induced biphasic aggregation of human platelets. 119 59

Autoradiographic tests carried out on rats with renal hypertension using 3H-proline resulted in an acclerated collagen synthesis by media cells of aorta and coronary arteries. Electronmicroscopically an increased content of collagen fibers and an enrichment of ruthenium-red-positive substances in the extracellular space were found. The 35S-sulfate-incorporation in aorta and coronary arteries of animals with hypertension is also increased. These changes in the extracellular space of the vascular wall have an atherosclerosis promoting effect, probably caused by a distrubance of the permeability.
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PMID:[Expermental contribution on the genesis of arteriosclerosis caused by hypertension]. 123 18

Diabetes mellitus is commonly associated with systolic and diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth-muscle cells. Physiological maneuvers, such as caloric restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; good evidence indicates that these maneuvers also can lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia also are associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate density and low-density lipoproteins, both of which are atherogenic. Last, insulin per se, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth-muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth-muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of a variety of growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including type II diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. 128 37

The relationship between blood pressure and platelet basal cytoplasmic calcium concentration ([Ca2+]i) and platelet sensitivity to aggregating agents in hypertension has been investigated in hypertensive patients and normotensive subjects. Ten severely hypertensive patients whose blood pressures were poorly controlled with metoprolol, were given calcium antagonist (either nifedipine or felodipine) as a second line agent. Venous blood samples were collected at each treatment phase for measurement, in whole blood, of platelet aggregation in response to ADP and collagen, and of basal [Ca2+]i using fura-2. Control of blood pressure by the combination of metroprolol and a calcium antagonist induced a significant decrease in median [Ca2+]i from 116 (76-181) to 73 (60-83) nM, which was similar to the median value of 70 (61-80) nM obtained in 14 normotensive subjects. Overall [Ca2+]i correlated with mean blood pressure (r = 0.51). Treatment of hypertension with calcium antagonist did not change the response of platelets to collagen or ADP. The results confirm that effective treatment of hypertension significantly reduced basal [Ca2+]i in platelets but raise doubts whether elevated basal [Ca2+]i is necessarily the sole mechanism by which the sensitivity of platelets to aggregatory agents is increased in hypertension.
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PMID:Treatment of hypertension induces a fall in platelet basal cytoplasmic calcium concentration without influencing platelet aggregation. 128 83

The data is presented on the pathogenesis of myocardial changes in arterial hypertension. The non-haemodynamic causes are discussed of myocardial hypertrophy, as well as the participation of collagen in its early phase and the haemodynamic consequences of hypertrophy and its regression. Hypotensive drugs and their ability ot prevent myocardial hypertrophy and (or) inducing of its regression were compared.
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PMID:[The heart in arterial hypertension]. 129 60


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