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

A review of the literature reveals a multitude of effects that noise may contribute to periodontal disease, including cardiovascular disease, angiospasm of peripheral vessels, hypertension, and an increase in inflammatory cells with concurrent inhibition of healing. Three groups of 25 men were selected from the Pennsylvania Air National Guard for study. Group 1 consisted of F-102 jet fighter pilots; Group 2, pilots and crew of a four-engine, propeller-driven C-121 aircraft; and Group 3, enlisted men not exposed to aircraft noise, as a control. The degree of alveolar, intraceptal bone loss for each subject was measured from full-mouth radiographs of all groups. The greatest amount of bone loss occurred in crew members of propeller-driven aircraft. Jet pilots had considerably less bone loss while the average number of millimeters of bone lost per tooth revealed a difference between the three groups to the 0.01 significance level (F=24.7). The data suggests there is a degree of alveolar bone loss over a period of years associated with exposure to propeller aircraft noise and vibration, and negligible loss for jet aircraft noise.
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PMID:Association of aircraft noise stress to periodontal disease in aircrew members. 116 37

The procedure for producing adrenal regeneration hypertension did not cause an increase in the systolic blood pressure of W/Fu animals. The regenerating adrenal gland in W/Fu animals was not restored to normal; reduced numbers of mitochondrial cristae were seen and the mitochondria were smaller in size; regeneration was complete in Sprague-Dawley rats of the Holtzman strain and there was a severe form of hypertensive, cardiovascular disease.
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PMID:Resistance of W/Fu rats to adrenal regeneration hypertension. 118 15

The demonstration that long-term administration of relatively low doses of clonidine decreased the responsiveness of blood vessels to vasodilator and vasoconstrictor drugs in animals led to its investigation in the prevention of migraine in man. Results of placebo-controlled and open therapeutic trials have shown that clonidine in low dosages (75 to 150 mug daily) is useful in preventing migraine headaches in about 30%-50% of patients. A 50% or greater reduction in headache frequency or headache indices has been reported in 40% of patients in controlled and open studies. Thus clonidine, like other drugs used in the interval therapy of migraine, can be expected to be effective in only a proportion of patients. Although clonidine has not been compared directly with other drugs used in the prophylactic treatment of migraine, the general clinical impression is that it is less effective then pizotifen or methysergide. Because it is relatively well tolerated at dosages of 75 to 150 mug daily it is worthy of a trial, particularly in patients considered to need prophylactic migraine therapy for the first time, and when migraine occurs in association with hypertension. At the dosages used in migraine prophylaxis, which are almost invariably lower than used in hypertension, clonidine does not cause hypotension and can be used in patients with cardiovascular disease. The principal side-effects are drowsiness and dry mouth which tend to diminish as treatment continues.
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PMID:Low-dose clonidine: a review of its therapeutic efficacy in migraine prophylaxis. 120 7

Hypertension was induced in young rats by latex encapsulation of both kidneys. By the fourth week, 85% of the renal-encapsulated (RE) rats became hypertensive. Varying degrees of cardiovascular involvement were evident in the moderately to severely hypertensive rats. The level of systolic blood pressure was directly correlated with the width and the volume of zona glomerulosa of the adrenal cortex. Electron microscopy combined with morphometric-stereologic techniques was employed to quantitate change in the adrenal cortex. The cells of both zona glomerulosa and zona fasciculata of RE rats showed significant increases in the volume of the cell, nucleus, smooth endoplasmic reticulum, and lipid droplets; only in the zona glomerulosa cells was the increase in surface area of the smooth endoplasmic reticulum statistically significant. It is suggested that these structural changes associated with renal-encapsulation hypertension are related at least in part to stress of the hypertensive cardiovascular disease.
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PMID:Quantitative ultrastructural study of the rat adrenal cortex in renal encapsulation-induced hypertension. 124 82

2 case histories of retinal damage in users of oral contraceptives (OCs) are discussed. The 1st, a 27-year-old woman who had used Eugynon for a year, had no history of cardiovascular disease of hemicrnaia. Ophthalmic examination showed vision in the right eye as less than 6/120, in the left 6/6, with indications of central serous chorio-retinpathy, with edematous center surrounded by small hemorrhages. After discontinuation of OCs, vision returned to 6/6 and paracentral scatoma disappeared. In the 2nd case a 37-year-old woman who had taken Eugynon and Ovulen for 1 year and Neolyndiol for 2 years complained of the appearance of a wedge-shaped shadow in her right eye. The patient had a history of metrorrhagia and hemicrania on the right side. Vision in both eyes was 6/6, but a paracentral scotoma in the right eye was present, a probable symptom of the patient's hypertensive spastic angiopathy. OCs were discontinued and propanol was administered, then discontinued due to symptoms of a scotoma in the left eye. The angiopathy disappeared but the ocular lesions remained. Ocular complications occur in about .07% of OC users. The damage results from arterial hypertension and changes in the macula lutea. Careful observation of blood pressure and ocular disturbances is the best preventative for ocular damage in OC users.
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PMID:[Retinal damage and oral contraceptives]. 125 82

The major target organs that suffer from sustained hypertension are the heart, kidneys, and brain. Cardiac adaptation to arterial hypertension consists of left ventricular hypertrophy (LVH) of the concentric type, that is, an increase in wall thickness at the expense of chamber volume. However, LVH can no longer be considered a simple adaptive myocardial process serving to compensate for the increase in afterload and bring left ventricular wall stress back to normal. Data from the Framingham cohort have shown that the occurrence of LVH drastically increases the risk of sudden death and other cardiovascular morbidity and mortality irrespective of the levels of arterial pressure. Renal adaptation to arterial hypertension consists of a decrease in renal blood flow with elevations in filtration fraction and renal vascular resistance. With progressive hypertensive cardiovascular disease, glomerular filtration rate will fall as well. Recent data in patients with mild-to-moderate hypertension demonstrate that despite "efficacious" antihypertensive therapy, one-third to one-half of hypertensive patients may experience a significant decline in renal function. Cerebrovascular adaptation to hypertension consists of micro- and macrovascular disease leading to vascular dementia, or ischemic or hemorrhagic stroke. Cerebrovascular autoregulation, the mechanism by which cerebral blood flow is maintained, despite changes in arterial pressure, may be altered in hypertension.
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PMID:End-organ disease in hypertension: what have we learned? 128 25

The association between blood pressure and coronary artery disease may be caused by a concurrence of atherogenic biochemical abnormalities in hypertensive patients, i.e., the metabolic cardiovascular syndrome (increased total cholesterol, triglycerides, and insulin; decreased high-density lipoprotein (HDL) cholesterol; and insulin resistance, glucose intolerance, and blood platelet dysfunction). There are numerous reports of sympathetic nervous system overactivity in hypertensive subjects that could be of importance for the pathophysiology of the high blood pressure. Plasma catecholamines have metabolic hormonal effects at concentrations slightly above low normal resting levels. Even transiently and certainly chronically raised plasma catecholamine levels may cause biochemical abnormalities. Catecholamines may raise total cholesterol, triglycerides, and insulin, decrease HDL cholesterol, and cause insulin resistance and glucose intolerance, and recent evidence supports an in vivo influence of epinephrine on blood platelets, causing dysfunction in hypertensive subjects. Thus, the sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension. Hypertensive subjects may respond to environmental stimuli with larger sympathoadrenal responses than normal subjects. Furthermore, emotional stress has been associated with coronary artery disease. Thus, the metabolic hormonal effects of catecholamines, by causing the metabolic cardiovascular syndrome, may be the crucial link between "stress" and cardiovascular disease.
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PMID:The sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension. 128 68

A short review of the metabolic cardiovascular risk syndrome (MCVS) is given. Traditionally, cardiovascular risk has been associated with three so-called "main" risk factors; hypercholesterolemia, hypertension, and smoking. In addition, the association between diabetes and cardiovascular disease has been known for many years in clinical medicine. Primarily, these risk factors have been regarded separately as independent factors, although epidemiological studies showed intercorrelations between them. However, it is now well accepted that relatively few at-risk individuals have only one risk factor, and in many cases a whole "symphony" of factors play together to create what we might call an individuals' risk profile. As an example, very often essential hypertension has been regarded as a disease in itself, which can be successfully treated just by lowering the blood pressure by drugs. When such a strategy obviously failed, the association of elevated blood pressure with dyslipoproteinemia and impaired glucose tolerance attracted more attention, particularly when it was realized that many antihypertensive drugs affected risk in MCVS in a possible negative way. The most important etiologic factor of MCVS is (besides genetics) an excessive caloric intake compared to what the individual spends in physical activity. In the clinical setting, the most important findings of MCVS are central obesity, dyslipoproteinemia with low high-density lipoprotein (HDL) cholesterol, hypertension, reduced insulin sensitivity in peripheral tissues, and increased thrombogenicity. The reduced insulin sensitivity leads to a compensatory increase in beta-cell insulin production, and thereby hyperinsulinemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The metabolic cardiovascular syndrome: syndrome X, Reaven's syndrome, insulin resistance syndrome, atherothrombogenic syndrome. 128 71

Hyperinsulinemia and insulin resistance have been implicated to play a role in the development of hypertension and to contribute to the increased risk for cardiovascular disease in diabetic, obese, hypertensive, and normotensive salt-sensitive humans. Reviewed herein are the effects of nonpharmacological measures, including exercise, weight loss, diet, and changes in lifestyle, on insulin resistance. Based on the evidence from both experimental and clinical studies, regular exercise, moderate weight reduction, and a low-fat, high-carbohydrate, high-fiber diet can markedly improve insulin sensitivity. The possible mechanisms involved are discussed. Because these nonpharmacological measures have also been shown to lower blood pressure and correct dyslipidemia, they can contribute substantially to the reduction of major cardiovascular risk factors and should be implemented in all patients who may be at risk for cardiovascular disease.
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PMID:Effects of nonpharmacological intervention on insulin sensitivity. 128 41

The outcome of untreated hypertension was investigated in a population of 17,713 persons in southern Taiwan who were aged 15 or over when they had taken part in a blood pressure survey in 1963. In the 27-year follow-up period, 55.8% of the overall mortality was comprised of those who were found to be hypertensive (as defined by WHO) in 1963, 31.3% by borderline hypertensives, and 22.6% by normotensives. The 27-year mortality rate due to stroke was much higher in hypertensives than in normotensives (11.4% vs 1.8%, respectively). The 5-year survival rates for mild, moderate and severe hypertensives were 89.9%, 82.7% and 72.3%, respectively, and the 20-year rates were 60.2%, 37.2% and 25.2%, respectively. The causes of death were also recorded: among hypertensives, stroke accounted for 23.2% of all deaths of known cause, cancer 20.5%, cardiovascular disease 21.7%, respiratory disease 11.8%, and other causes 22.9%. From the results, it is concluded that obvious differences in mortality and cause of death exist between untreated hypertensives and normotensives.
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PMID:Outcome among untreated hypertensives in the general population in Taiwan. 128 80


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