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

Echocardiographic dimensions and hemodynamic indexes were determined in 42 patients with borderline hypertension and in 22 with sustained hypertension and the results were compared with findings in 33 normal subjects. In patients with borderline hypertension the thickness of the interventricular septum (IVS) was significantly increased (P less than 0.001), whereas the posterior wall PW) thickness remained within normal range. The IVS/PW ratio was significantly elevated (P less than 0.001) and was correlated negatively with the cardiac index (P less than 0.01) and positively with the preejection period (P less than 0.01). In patients with sustained hypertension a symmetric cardiac hypertrophy was observed, and there was a significant positive correlation between the IVS/PW ratio and diastolic pressure (P less than 0.05). The study suggested that (1) in sustained hypertension the symmetric cardiac hypertrophy was secondary to a progressive increase in pressure load, whereas (2) in borderline hypertension the asymmetric cardiac hypertrophy could not be directly related to the level of blood pressure and was probably associated with abnormalities of the sympathetic nervous system.
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PMID:Echocardiographic dimensions in borderline and sustained hypertension. 15 66

Borderline hypertension attracts investigative interest since it is an early predictor of established hypertension and its sequelae. This condition offers the opportunity of studying arterial hypertension at its inception, before the development of secondary pressure-related changes. A number of abnormalities of the circulation have been described in borderline hypertension. The peripheral resistance is either elevated or inappropriately adjusted to the prevailing increased cardiac output and blood flow. Cardiac output, heart rate and stroke volume are elevated in a proportion of patients. Decreased plasma volume, enhanced pressor responsiveness and elevated plasma renin activity have also been noted. All these changes could hypothetically be explained by a neurogenic mechanism. Although the experimental evidence supporting a neurogenic origin of borderline hypertension is incomplete and often indirect, most findings point toward an abnormal autonomic control of the circulation in this disorder. It is postulated that in a subgroup of patients with borderline hypertension a neurogenic mechanism is in fact operative. There is a need for further characterization of this category of borderline hypertension and for description of its natural history, particularly in relation to the possible subsequent development of essential hypertension.
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PMID:Autonomic nervous cardiovascular regulation in borderline hypertension. 17 39

1. Urinary kallikrein was measured in 67 patients with essential hypertension and 25 normotensive subjects variously on unrestricted and low sodium diet. Also, the effect of orally applied hog pancreatic kallikrein on elevated blood pressure and kallikrein excretion was evaluated. 2. Urinary kallikrein was reduced in a large subgroup of patients with sustained essential hypertension. 3. With salt restriction, urinary kallikrein rose markedly in normotensive subjects and patients with borderline hypertension but not in those with sustained hypertension. 4. Oral kallikrein normalized reduced kallikrein excretion and lowered elevated blood pressure. 5. The rise in urinary kallikrein with oral kallikrein was due to an increased formation of endogenous enzyme. 6. A defective kallikrein-kinin system may be involved in both the low urinary kallikrein excretion and the hypertension.
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PMID:Low urinary kallikrein excretion and elevated blood pressure normalized by orally kallikrein in essential hypertension. 26 17

Seven hundred and fifty asymptomatic European subjects aged 16 to 69 years from an urban general practice were screened for various coronary risk factors. Required information was completed for 98.9 percent of the total sample. The incidence of individual risk factors in males and females respectively were: smoking, 52.8 percent and 45.6 percent; obesity, 26.9 percent and 30.9 percent; definite hypertension, 5.6 percent and 4.0 percent; borderline hypertension, 5.3 percent and 5.1 percent; hyperlipidaemia, 12.8 percent and 8.0 percent; impaired glucose tolerance, 1.1 percent and 1.3 percent. Respective figures for males and females with regard to numbers of risk factors present were: one or more risks present, 68.5 percent and 66.9 percent; two or more, 26.5 percent and 23.5 percent; three or more, 8.0 percent and 4.5 percent; four risk factors present, 1.6 percent and 0.3 percent.
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PMID:Distribution of various coronary risk factors in an urban general practice. 27

Essential hypertension is a quantitative abnormality, the pathological effects and risks increasing with the blood pressure level. In Western countries blood pressure rises with age in most individuals, so essential hypertension is more frequent in middle and older age groups. It is likely that an individual's blood pressure level is determined by many interacting factors. These include heredity, which probably acts multifactorially, and many environment influences, including psychological stress and obesity. Specific factors may be of varying importance in different individuals and in different populations. Several physiological mechanisms control the blood pressure level and may be altered in essential hypertension. In early hypertension sympathetic nervous activity is sometimes increased, although in long-standing hypertension this is less marked. Cardiac output may be increased in borderline hypertension but is normal in established hypertension, when total peripheral resistance is increased. Total exchangeable sodium is normal, while the renal pressure-natriuresis balance is altered, so that for a given pressure the hypertension kidney excretes less sodium. In some patients, plasma renin is low, probably as a result of renal adaption to prolonged hypertension. The pathogenic sequence in essential hypertension is uncertain. Increased autonomic activity may cause vasoconstriction in renal and other arterioles and increase cardiac output, leading to a rise in blood pressure. Elevated pressure itself produces structural changes in the resistance vessels, including those of the kidney, which eventually maintain the hypertension even when the initiating stimulus is removed. The way in which heredity and environment influence pathogenic mechanism is also uncertain. Heredity might, for example, influence the autonomic response to stress or the liability to irreversible changes in the resistance vessels or in the kidney. Environmental factors may also increase autonomic activity, enhance vascular reactivity or alter renal function.
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PMID:The pathogenesis of essential hypertension. 40 33

Systemic hemodynamics (cardiac output, intraarterial pressure, total peripheral resistance) and intravascular volume (plasma volume and red cell mass) were measured in a population of 126 black and white patients, 51 with borderline hypertension and 75 with established essential hypertension. The findings were compared with those in 29 age-matched normotensive control subjects of both races. The white patients with established hypertension demonstrated a faster heart rate than the black patients (less than 0.05); this difference was more pronounced during upright tilt (p less than 0.02). No significant difference in cardiac index, total peripheral resistance, plasma volume or total blood volume was found between the two racial populations. Cardiac index correlated directly with plasma and total blood volume in black patients (r = 0.32, p less than 0.05) and white patients (r = 0.35, p less than 0.001) as well as in the whole study population (r = 0.36, p less than 0.001). The regression lines were similar in the two races. Further, a negative correlation was observed between the total peripheral resistance and plasma volume (r = -0.31, p less than 0.001) or total blood volume (r = -0.34, p less than 0.001), and it was similar in both races (blacks r = -0.48, p less than 0.01; whites r = -0.25, p less than 0.05). Age correlated significantly with total peripheral resistance in the white patients (r = 0.35, p less than 0.001) and in the total study population (r = 0.28, p less than 0.001). We conclude that, for every given age or level of arterial pressure, systemic hemodynamics are similar for the black and white patients with essential hypertension. These data, therefore, do not support the clinical impression that basic pathophysiology and hypertensive vascular disease are different in the black patient with essential hypertension.
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PMID:Essential hypertension in black and white subjects. Hemodynamic findings and fluid volume state. 46 13

Marginal blood pressure elevation at youth is widely prevalent. Clinically such patients represent a dilemma, since they are at highest risk to develop hypertension and its sequelae, but the risk is not sufficiently strong to mandate antihypertensive medication. The decision as to whether to treat will depend on the presence of other risk factors for hypertension. Multiple and complex pathophysiologic abnormalities have been described in borderline hypertension. A better understanding of the relationship of some of these abnormalities to the development of hypertension is needed.
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PMID:Clinical and physiological significance of borderline hypertension at youth. 62 67

The occurrence of the C3F allele was investigated in the following three groups: 69 consecutive referred patients with untreated essential hypertension, including borderline hypertension; 70 patients with established and treated essential hypertension, already attending the same outpatient clinic, and 62 age- and sex-matched normotensive healthy subjects without clinical signs of atherosclerosis or familial predisposition to hypertension. In the three groups the C3F allele was found in 38.2%, 29% and 20%, respectively. Among the treated hypertensive patients with C3F gene, 40% had coronary heart disease (CHD) compared to 6.1% among the C3F negative (P less than 0.005), and the relative risk of CHD among the treated hypertensive patients with this allele was found to be 10.2 (P less than 0.002). The C3F gene was present in 72.7% of the treated patients with CHD. In the untreated patients the occurrence of CHD was low, and no differences between C3F positive and negative patients could be demonstrated. No association of the C3F allele with familial predisposition to hypertension was found. This study provides further evidence of a positive association of the C3F allele with atherosclerosis, and it is concluded that this allele in a hypertensive patient might accelerate the atherosclerotic process, with subsequent premature development of vascular complications.
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PMID:Association between coronary heart disease and the C3F-gene in essential hypertension. 68 71

Borderline hypertension is widespread. Though the increased blood pressure appears to be innocent, and upon rest frequently returns to the normal range, signs of complex and profound alteration of the physiologic control of the circulation can already be found. The pathophysiology of borderline hypertension is of particular interest since it may reveal clues about the processes which initiate the hypertension rather than the consequences of the primary blood pressure elevation. Patients with borderline hypertension are at a higher risk of developing future sustained hypertension and its consequences. The risk, however, is not sufficient to justify treatment in all cases. Patients must be followed to observe blood pressure trends and treatment attempted in the selected minority which has the highest risk. The determination of risk is based on repeated measurements of blood pressure and on the assessment of risk factors for atherosclerosis and for future hypertension.
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PMID:Borderline hypertension. An overview. 85 4

Daily s.c. injections of 0.02--10.0 mg angiotensin in depot form for 14 days caused in rats, under defined conditions, pronounced dose-dependent effects, with an unusual tolerance to the drug being observed. The behaviour of the systolic and diastolic blood pressure and heart rate allowed to define 4 dose ranges. In the lowest dose range of 0.02 mg angiotensin-II a lasting borderline hypertension with only straight-line changes of diastolic blood pressure and bradycardia were observed. The doses of 0.15--1.25 mg angiotensin-II caused a continual blood pressure rise and led, between day 4 and 6 of the experiment, to a pronounced lasting resistance high-pressure without appreciable changes in heart rate. The strongest resistance high-pressure, which occurred as early as on day 3, with pronounced tachycardia was achieved with a dose of 2.5 mg angiotensin-II. Higher doses produced pronounced tachycardia but no significant effects on blood pressure. The varying dose-dependent effects of depot angiotensin are discussed, and the possibility is pointed out to study by the angiotensin-II hypertension model various mechanisms of a long-time hypertensive dysregulation.
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PMID:[Studies on the blood pressure effects of various high doses of angiotensin II in depot form in rats under defined conditions]. 101 70


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