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

The variability of blood pressure measurements is studied, in a standardized screening, by comparing the measures obtained during a medical examen and those made by technicians under different circumstances. This variability is important. A systematic bias is due to the digit preference for the zero value by the doctors. Besides, strong subject/obser interaction accounts partly for higher values measured in the medical exam. The mean blood pressures and the prevalence of hypertension are increased under some circumstances close to those of everyday life and labile hypertension is very frequent. The individual variability of the measure and the prevalence of hypertension are reduced by a standardized technique when applied under favorable circumstances by technicians. The reproductibility of this measure is good but the simultaneous taking into account of two successive measures still reduces much this prevalence. In these conditions it is very difficult to estimate the prevalence of hypertension in the population: an example is given where this frequency varies in the proportion of 1 to 6 according to the measures considered. The implications of this variability on the screening of hypertension are discussed.
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PMID:[Variations in blood pressure measurement during systematic screening tests and their effects on public health]. 12 Jul 20

The Frank-Starling relationship of hearts from adult spontaneously hypertensive rats (SHR, Okamoto 1969), representing the established phase of hypertension, and of young SHR, representing the initial phase of hypertension, was investigated by using the isolated working heart preparation. In the "normal" diastolic pressure range (5 to 10 cm H2O), the left ventricle of both SHR groups displayed significantly reduced stroke volumes compared with hearts of normotensive controls (NCR); the degree of reduction being proportional to the left ventricular hypertrophy. This is suggested to be due to a reduced left ventricular diastolic compliance in SHR, as indicated by direct measurements of ventricular wall thickness and end-diastolic volumes in arrested hearts exposed to different end-diastolic filling pressures. Such a progressive shift of the Frank-Starling relationship to the right with duration of hypertension could, in combination with the gradual development of "structural autoregulation" of the precapillary resistance vessels, constitute dominating factors in shifting the hemodynamic situation in labile hypertension into that characterizing the established, or "fixed", state of hypertension.
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PMID:Consequences of myocardial structural adaptation on left ventricular compliance and the Frank-Starling relationship in spontaneously hypertensive rats. 12 25

Labile hypertension in patients under 50 years of age (the non-atherosclerotic form) was found to be characterized by higher urinary excretion of catecholamines and particularly of homovanillic acid; when further analyzed it was shown to be a heterogeneous entity with two types of patients clinically and biochemically distinguishable from each other, from control subjects and from patients with stable hypertension. Reactivity to assuming an upright posture distinguishes one type of labile hypertension having a normal postural pulse rate response from another having an excessive postural increase in pulse rate. The first group also showed normal responses of plasma norepinephrine concentration and of urinary cyclic AMP to posture. The group with excessive pulse rate response, in contrast, showed a decrease in plasma norepinephrine and an excessive increase of urinary cyclic AMP excretion in response to upright posture. The results suggest that not only circulating catecholamines but also the reactivity of their target tissues (as probably reflected by cyclic AMP measurements) are important in bringing about signs of adrenergic excess. The hypothesis that cyclic AMP changes reflect beta-adrenergic receptor reactivity is strongly favoured by data indicating qualitative differences in cyclic AMP responses to beta-adrenergic stimulation or inhibition between control subjects and those labile hypertensive patients with clinical signs of excessive sympathetic reactivity. The study stresses the need for more precise definition of labile hypertension, for dynamic clinical and biochemical correlative studies, and for consideration not only of the circulating hormones but also of the "second messengers" (such as cyclic AMP and cyclic GMP) which reflect the cellular action of hormones. Blood pressure is a very labile parameter in health and disease. In one sense, therefore, hypertension can be considered "labile" in every hypertensive patient. Usually, however, labile (or borderline) hypertension is regarded as characterized by a blood pressure over 140/90 mmHg, falling below these values with physical and emotional rest. This clinical entity, which affects some 20% (variously estimated between 16 and 30%) of the adult population, gives rise to uncertainties in both definition and prognosis. In some patients labile hypertension represents the precursor of a fixed hypertensive state, whereas in many others it remains labile throughout life, never progressing to the stable phase nor becoming associated with hypertensive cardiovascular disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Labile (borderline) hypertension--new aspects of a common disorder. 23 54

Neurohumoral mechanisms operating via the catecholamines are discussed in their relationship to such hypertensive diseases as pheochromocytoma and labile and established essential hypertension. 2. In pheochromocytoma, diagnosis depends almost entirely on identification of increased amounts of catecholamine metabolites in the urine. Because of the danger, manipulative or invasive procedures both for diagnosis and during surgery should be kept at a minimum. 3. In established essential hypertension, reactivity to norepinephrine and plasma norepinephrine are increased, whereas norepinephrine uptake and apparent secretion rate are decreased. 4. In labile essential hypertension, reactivity to epinephrine and probably plasma epinephrine are increased and uptake of epinephrine decreased. 5. Labile hypertension with all its characteristics may or may not coexist with established essential hypertension with all its features. 6. The sympathetic nervous system is also involved in other types of hypertensive disease. Many patients with renovascular hypertension as well as with primary and secondary hyperaldosteronism also have essential hypertension. Angiotensin II affects the sympathetic nervous system and the juxtaglomerular apparatus appears to be beta adrenergic receptor activated, at least in part.
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PMID:Neurohumoral mechanisms in hypertension. 23 64

Essential hypertension is increasingly recognized as a nonhomogenous disorder by various methods of study. The hemodynamic approach, coupled with clinical determination of the range and lability of blood pressure, has resulted in the description of several subgroups: labile hypertension with normal or elevated cardiac output, fixed or established hypertension with varying cardiac output and advanced hypertension with normal or low cardiac output. There is a tendency to postulate that these categories are stages of one disorder, but this remains to be proved. Still other patients have been described who may be further set off by exceptionally labile or hyperkinetic features. In some hypertensive patients, the peripheral resistance is normal; however, regardless of its numerical value, it is now considered to be increased if it fails to decrease normally in the presence of elevated cardiac output. Because an elevated cardiac output is the hemodynamic function that differentiates these groups, and renovascular hypertension as well, it is the focus of much current work. New interest in the central blood volume, the peripheral veins, and the portal veins and splanchnic circulation is focused on their connection with cardiac out-put. Newly appreciated, too, is the existence of parasympathetic inhibition in hypertension, which not only contributes to elevations of heart rate, cardiac output and possibly renin secretion, but also depresses baroreflex responses. Thus far, hemodynamic and endocrine mechanisms of hypertension have not been studied together, except possibly through the blood volume, which remains a highly controversial topic. In this paper, some recent work in the above areas is reviewed and emphasis is given to studies in man.
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PMID:Hemodynamic lesions in hypertension. 24 10

1. Average supine circulating total catecholamine concentrations were found to be higher than the normal range in about 50% of patients with labile hypertension and in about 30% of patients with sustained essential hypertension. 2. These higher resting concentrations were mainly due to an increase in adrenaline in labile hypertension and to an increase in noradrenaline in sustained hypertension. 3. Patients with elevated catecholamine concentrations were also characterized by a higher heart rate, by an increased myocardial contractility and by greater hypotensive response after treatment with beta-adrenoreceptor blocking agents. 4. These studies suggest the existence of sub-groups of hypertensive patients with increased sympathetic tone.
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PMID:Circulating catecholamines and systolic time intervals in labile and sustained hypertension. 28

Kallikrein excreted with the urine appears to be formed in the kidney. The kallikrein-kinin system in the kidney is localized in the distal nephron from the juxtaglomerular apparatus to the collecting duct. It has been shown that intrarenal infusion of kinins produces an increase in renal blood flow as well as diuresis and natriuresis. Part of the effect of kinins appears to be mediated by the release of prostaglandins. However, the precise role of the renal kallikrein-kinin system in sodium and volume homeostasis and in blood pressure regulation still remains to be determined. Mineralocorticoids as well as the diuretics furosemide, bumetanide and bendroflumethiazide increase, spironolactone decreases kallikrein excretion. Urinary kallikrein has been shown to increase acid-as well as cryoactivation of prorenin in vitro. It is unclear as yet, however, whether the renal kallikrein-kinin system takes part in converting inactive prorenin into active renin in vivo. There are reports on subnormal, normal as well as increased kallikrein excretion in spontaneously hypertensive rats. In rats susceptible to the hypertensive effect of salt a substantially decreased excretion of kallikrein has been observed. Kallikrein excretion has been described to be increased in primary aldosteronism and to be reduced in a proportion of patients with established essential hypertension. In patients with labile hypertension, however, kallikrein excretion appears to be normal suggesting that decreased urinary kallikrein in essential hypertension is a consequence rather than a cause of hypertension. The renal kallikrein-kinin system does not appear to play a primary role in the pathogenesis of hypertension.
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PMID:[Renal kallikrein-kinin system and control of blood pressure (author's transl)]. 39 77

Reserpine was administered in purpose to determine the "Noradrenaline store" in sympathetic nerve endings. The marked increase of urinary noradrenaline excretion was observed by reserpine 0.4 mg/day administration. Total amount of noradrenaline in urine for first three days of 0.4 mg/day of reserpine administration was considered as a good indicators of "Noradrenaline store". There was no difference of "Noradrenaline store" between normal and hypertensive subjects. The increase % of urinary noradrenaline was higher in labile hypertension than in established hypertension as well as in normal subjects. Though the relationship between "Noradrenaline store" or the increase % of noradrenaline and sympathetic nerve activity was not clear, it is suspected that the releasable noradrenaline in sympathetic nerve granule was higher in labile hypertension than in established hypertension or normal subjects.
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PMID:Response of urinary noradrenaline excretion to reserpine administration in normal and hypertensive subjects. 50 5

1. Intralymphocytic sodium concentration was measured in 50 patients with essential stable hypertension, 44 patients with labile hypertension and 40 subjects with normal blood pressure. 2. Intralymphocytic sodium concentration in normotensive subjects was significantly lower than in the other two groups. 3. The concentration was significantly correlated with mean blood pressure in the group as a whole and in the groups with stable and with labile hypertension. No correlation was found in normal subjects.
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PMID:Intralymphocytic sodium in hypertensive patients: a significant correlation. 54 Apr 50

The hemodynamic response to mental stress (mental arithmetic) was studied in adolscents with varying risk factors for essential hypertension (EH), One group (genetic) consisted of normotensive well adolescents who had at least one parentnt with EH. Another group (labile) consisted of adolescents with labile hypertension each of whom also had at least one pare with EH. The control population consisted of normotensive adolescents with a negative family history of EH. Subjects with labile hypertension demonstrated a sustained increase in systolic and diastolic pressure and heart rate during stress. This response was significantly different than the control population (P less than THE CONTROL POPULATION (P LESS THAN 0.001). The stress response of the normotensive genetic population was qualitatively similar to the group with labile hypertension and significantly different than the controls in diastolic pressure and heart rate (p less than 0.001, less than 0.02). Post-stress plasma catecholamines were higher in the labile hypertensive and genetic groups than in the control group. These findings demonstrate increased central nervous system mediated adrenergic activity and cardiovascular response in labile hypertension and also in some normotensive subjects with a genetic risk for hypertension.
Hypertension
PMID:Cardiovascular response to mental stress in normal adolescents with hypertensive parents. Hemodynamics and mental stress in adolescents. 54 10


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