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

The relation of plasma dopamine beta-hydroxylase (DBH) activity to age was examined in normotensive and hypertensive subjects. Plasma DBH activity was the highest in the group of 25--34 years and gradually decreased with age. Plasma DBH activity was higher in the hypertensives than in the normotensives in all age groups, and the difference was significant between the groups of 45--54 and 55--64 years. Plasma DBH activity was increased in labile hypertension. Plasma DBH activity was higher in the group of essential hypertension with normal renal function than in that with reduced renal function. It was lower in the severe hypertensives than in the mild cases. Plasma DBH activity was also decreased in the hypertensive patients with cerebrovascular disorders. Plasma DBH activity was lower in the hypertensive patients with renal parenchymal diseases than those of essential hypertension with normal renal function. Plasma DBH activity was also decreased in primary aldosteronism, while it was increased in pheochromocytoma. These observations suggest that measurement of plasma DBH activity may be valuable in the differentiation of essential hypertension from the secondary forms of hypertension, and the evaluation of the hypertensive processes. To evaluate plasma DBH activity, it is important to consider its age-related changes.
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PMID:The evaluation of plasma dopamine beta-hydroxylase activity in essential and secondary hypertension. 57 40

Plasma adrenaline, noradrenaline, and dopamine concentrations and plasma renin activity were measured in the supine position and after standing for 10 minutes in 14 patients with sustained benign essential hypertension and in five patients with labile hypertension. Results were compared with values obtained in 11 normotensive control subjects. In controls plasma noradrenaline concentrations increased with age, while plasma adrenaline values tended to decrease with age. No significant difference in mean plasma noradrenaline was found between hypertensive and control subjects, but plasma noradrenaline seemed slightly increased in a proportion of hypertensive patients aged less than 50. Plasma adrenaline was considerably raised in both supine and standing positions in eight patients with sustained hypertension and in two with labile hypertension. Dopamine concentrations and plasma renin activity were similar in all groups studied. The finding of significantly raised plasma adrenaline concentrations in a large proportion of hypertensive patients supports the hypothesis that the activity of the sympathetic nervous system is increased in essential hypertension. Measurement of plasma adrenaline seems to be a more sensitive index of this activity than that of plasma noradrenaline.
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PMID:Increased plasma adrenaline concentrations in benign essential hypertension. 58 24

Arterial pressure was continuously recorded for 24--48 h in 3 normotensive subjects and in 60 hypertensive patients. The greatest variations occurred in those with labile, mild or moderate hypertension compared to those with severe hypertension or normal blood pressure. Atenolol (100-200 mg) administered once or twice daily produced a significant reduction of arterial pressure and a smaller response to the cold pressor test, hand grip and step test in patients with established hypertension, but little change in those with labile hypertension. The evening dose was not followed by a decrease in pressure greater than that observed without treatment, but determined a smaller rise on awaking.
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PMID:Circadian variations of blood pressure in patients with different degrees of hypertension. Changes induced by hypotensive treatment. 61 45

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

In a study of 138 patients with diabetic retinopathy and good fluorescein angiograms, areas of CNP were found in 66.5% using a macular centered photograph. There was no statistically significant correlation between the appearance of CNP, their size and number with the level of systolic and diastolic blood pressures, the duration of diabetes (at the onset of diabetic retinopathy), the age at onset of diabetes, the age at examination, the control of the diabetes and the treatment of hypertension. The only borderline statistically significant difference was found between patients with constant hypertension when compared to patients with labile hypertension.
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PMID:Retinal ischemia (capillary nonperfusion) in diabetic retinopathy of patients with and without systemic hypertension. 74 25

Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) Changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that 'noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem' (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-beta-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ('adaptive metabolic change', Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development of hypertension (neurovascular linkage, Yamori, 1975)...
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PMID:Pathogenesis of spontaneous hypertension as a model for essential hypertension. 87 Jul 22

The population of a community of 29,608 adults was screened door-to-door for elevated blood pressure. Of 12,371 adults screened, 20% were classified as hypertensive. After repeated blood-pressure measurement, however, there were only 9% with sustained hypertension, while 11% had labile hypertension. Sixty percent of the cases of sustained hypertension had been either undiagnosed, untreated, or inadequately treated. Eighty-two percent who initially were unaware of hypertension had labile hypertension after repeated blood-pressure measurement, and 18% were unaware of having, sustained hypertension. Labile hypertension was most prevalent in the young and decreased with age. In contrast, sustained hypertension was least prevalent in the young and increased with age. Labile hypertension was most prevalent in white men, and sustained hypertension was more prevalent in blacks than in whites. Labile hypertension represents a large segment (52%) of the population initially identified as having hypertension in a home blood-pressure survey.
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PMID:The Charlottesville Blood-Pressure Survey. Value of repeated blood-pressure measurements. 94 65

Rats treated neonatally with angiotensin showed labile hypertension in adulthood. This finding may suggest a permanently changed responsiveness of a central nervous controller of the cardiocirculatory system caused by angiotensin-induced hypertension during brain differentiation.
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PMID:Hypertension in adult rats treated neonatally with angiotensin. 100 4

Haemodynamic studies were made on 31 patients with labile hypertension at rest and during exercise. Plasma renin activity (PRA) was measured in 8 of them. Five haemodynamic types could be recognised and they could be arranged into two groups. The first was characterised by an increase of calculated peripheral resistance, sometimes permanent, sometimes revealed by effort, sometimes in relation to an increased cardiac output; this would appear to predict the development of permanent hypertension. The second group was characterised by normal systemic resistances, adapted to the cardiac output which was either normal or increased; the significance of labile hypertension in these cases was uncertain; from the haemodynamic studies one was unable to distinguish a transient emotive hypertension from potential permanent hypertension. The PRA was raised in the supine position and greatly increased by an orthostatic posture in the 8 patients tested, suggesting therefore an underlying neuro-adrenergic mechanism. In some patients with labile hypertension the haemodynamic tests were normal at rest and during effort. Others had different responses, which may be the result of varieties of hyper-sympathetic activity, either pure or predominantly beta-adrenergic (increased cardiac output, peripheral resistance adapted to the output) or combined beta and alpha (increased cardiac output with raised peripheral resistance) or mainly alpha-adrenergic (normal cardiac output, increased peripheral resistance).
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PMID:Haemodynamic diversity and plasma renin activity in labile arterial hypertension. 108 32

Urinary excretion of dopamine, norepinephrine and homovanillic acid was measured in normotensive subjects and in patients with either labile of stable hypertension under conditions controlled for posture, sodium and potassium intake and time of day. Mean homovanillic acid excretion was 313.5 plus or minus 77.7 (SE) mug/4h in the normotensive patients. Mean values for the patients with labile or stable hypertension were significantly greater, at 2506 plus or minus 476 mug/4 h (P smaller than 0.001) and 795 plus or minus 170 mug/4 h (P smaller than 0.01), respectively. Urinary excretion of dopamine and norepinephrine tended to be elevated in patients with labile hypertension when compared with values in the control subjects and the patients with stable hypertension. The data are compatible with the hypothesis of adrenergic hyperactivity in labile hypertension and underline the biochemical heterogeneity of essential hypertension. Because the overlapping of values between control subjects and patients with labile hypertension was minimal, it is proposed that an elevated valve for urinary homovanillic acid could be used as a biochemical marker to identify the patients with labile hypertension.
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PMID:Urinary homovanillic acid, dopamine and norepinephrine excretion in patients with essential hypertension. 111 92


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