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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with essential hypertension can be subdivided into groups with low (19%), normal (59%) or high (23%) renin sodium index. The proportion with low renin hypertension increases with age. Patients with high renin fall in two categories: younger patients with fairly mild hypertension and older patients with more severe hypertension and signs of renal disease. The antihypertensive efficacy of betablocker monotherapy is best in high renin forms, good but less consistent in normal renin patients and uniformly bad in low renin hypertensives. In relation to age, betablockers normalized blood pressure (less than or equal to 95 mm Hg diastolic) in three-quarters of the younger-than-40-year-olds, in about half of those 40-60 years of age but in only 20% of those over 60 years. On this basis, it is postulated that the older patients with a low renin exhibit a relatively hypoadrenergic state whereas those with a normal or high renin--for a given age and elevated pressure--have a relatively increased adrenergic nervous activity. Because the betablockers have a potent suppressive action on the renin-angiotensin system--and, as a consequence, on angiotensin vasoconstriction, aldosterone volume expansion and central stimulatory feedback mechanisms--their antihypertensive mode of action may be linked to an important extent, although not exclusively, to renin suppression.
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PMID:Renin and age as determinants of a predominantly betablocker-based antihypertensive drug program. 1 85

From analyses of the effectiveness of beta-blocker monotherapy in relation to the patient's age and to pre-treatment renin determinations an antihypertensive drug program is proposed in which beta-blockers form the cornerstone. Patients with essential hypertension can be subdivided into groups with low (19%), normal (59%), or high (23%) renin sodium index. The proportion with low renin hypertension increases with age. Patients with high renin fall into two categories: younger patients with fairly mild hypertension and older pateients with more severe hypertension and signs of renal disease. The antihypertensive efficacy of beta-blocker monotherapy is best in high renin forms, good but less consistent in normal renin patients and uniformly bad in low renin hypertensives. In relation to age, beta-blockers normalized blood pressure (larger than or equal to 95 mmHg diastolic) in three-quarters of the younger than 40-year-olds, in about half of those aged 40--60 years, but in only 20% of those aged over 60 years. On this basis, it is postulated that the older patients with a low renin exhibit a relatively hypoadrenergic state while those with a normal or high renin--for a given age and elevated pressure--have a relatively increased adrenergic nervous activity. Because the beta-blockers have a potent suppressive action on the renin-angiotensin system--and, as a consequence, on angiotensin vasoconstriction, aldosterone volume expansion and central stimulatory feedback mechanisms--their antihypertensive mode of action may be linked to an important extent, though not exclusively, to renin suppression.
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PMID:A beta-blocker-based antihypertensive drug program guided by age and renin. 1 22

1. In seventeen patients with untreated essential hypertension the sodium and water contents of leucocytes were significantly increased, whereas the rate constant for ouabain-sensitive sodium efflux was significantly reduced. 2. These abnormalities were not found in fourteen other patients with well-controlled hypertension. 3. Preliminary observations in accelerated hypertension suggest a different pattern of abnormality in leucocyte sodium metabolism.
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PMID:Abnormal sodium transport in leucocytes from patients with essential hypertension and the effect of treatment. 2 75

To investigate the initial potassium loss and development of hypokalaemia during the administration of an oral diuretic, metabolic balance studies were performed in ten patients with essential hypertension who had shown hypokalaemia under prior oral diuretic treatment. Chlorthalidone (50 mg daily) was given for 14 days. Six patients received a normal-sodium diet and four a low-sodium (17 mmol/day) diet. All patients had a normal initial total body potassium (40K). The electrolyte balances, weight, bromide space, plasma renin activity, and aldosterone secretion rate were measured. In both groups a potassium deficit developed, with proportionally larger losses from the extracellular than from the intracellular compartment. In the normal-sodium group the highest mean potassium deficit was 176 mmol on day 9, after which some potassium was regained; in the low-sodium group the highest deficit was 276 mmol on day 13. The normal-sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low-sodium group renin and aldosterone increased more slowly but remained elevated. It is concluded that dietary sodium restriction increases diuretic-induced potassium loss, presumably by an increased activity of the renin-angiotensin-aldosterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion.
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PMID:Initial potassium loss and hypokalaemia during chlorthalidone administration in patients with essential hypertension: the influence of dietary sodium restriction. 2 52

In 22 patients with essential hypertension plasma levels and urine excretions of sodium and noradrenaline were studied before, during and after long-term beta-blockade with pindolol. The relation between mean blood pressure and the quotient of sodium-/noradrenaline-excretion changed during treatment (placebo r=-0.34; pindolol r=+0.31). During placebo there existed a significant (p is less than 0.03) correlation between blood pressure and sodium-excretion which disappeared during beta-blockade. No correlation between blood pressure and noradrenaline was seen during placebo, whereas during beta-blockade a significant (p is less than 0.003) correlation was observed. In contrast to the placebo period there was a significant positive correlation between sodium- and noradrenaline-excretion during long-term treatment with pindolol. It is concluded that whole-body balance of sodium and noradrenaline is an important factor in essential hypertension.
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PMID:[The importance of changes in whole-body balance of sodium and noradrenaline in essential hypertension (author's transl)]. 3 Aug 56

Recent research shows that the renin-angiotensin-aldosterone axis either maintains or causes some or all of the high blood pressure of most patients and demonstrates anew that renin-sodium profiling defines this involvement. Performed with a serum potassium measurement, this now reliable test is useful for primary screening and then, in conjunction with renal vein renin studies or an aldosterone profile, for diagnosis or exclusion of surgically curable renovascular or adrenocortical hypertensions. For the remaining majority with essential hypertension, renin profiling exposes the relative participation of either vasoconstriction or volume factors, thereby guiding simpler, more specific, and predictably effective antirenin or antivolume treatments. Renin profiling identifies those in whom treatment should begin with a beta-blocker as opposed to a diuretic while not infrequently also providing baseline information about severity and prognosis in individual patients.
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PMID:Renin profiling for diagnosis and treatment of hypertension. 3 92

A study of the frequency distribution of plasma-renin concentration in 81 patients with essential hypertension produced no evidence of a distinct sub-population with low renin levels. An arbitrary dividing line was used, therefore, to define low-renin hypertension (36% of patinets). Patients in this group were older than those with normal renin levels, and there was a significant negative correlation between renin and age among all patients. Low-renin hypertension was not characterized by increased exchangeable sodium, but exchaneable postassium was significantly lower than in patients with normal plasma-renin. This difference became insignificant when five patients in the low-renin group with persistent hypokalaemia were excluded. It is concluded that low-renin hypertension does not represent a separate diagnostic entity but that plasma-renin falls with age in essential hypertension.
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PMID:Is low-renin hypertension a stage in the development of essential hypertension or a diagnostic entity? 4 18

Cation transport and electrolyte composition were studied in leucocytes from 17 patients with uncomplicated essential hypertension. Significant increases in cell sodium and water contents, associated with a depression of the rate-constant for active sodium efflux, were found in the hypertensive patients. These abnormalities in cell sodium transport may possibly be related to mechanisms of hypertension.
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PMID:Abnormal leucocyte composition and sodium transport in essential hypertension. 4 73

Parallel fluctuations of potential difference (P.D.) across oral and rectal mucosa are probably related to the activity of autonomic nerves rather than adrenal steroids. Unlike rectal mucosa, oral mucosa does not respond to exogenous or endogenous aldosterone. Therefore subtraction of oral P.D. from rectal P.D. gives a closer indication of mineralocorticoid activity than does rectal P.D. alone. In normal subjects plasma-aldosterone correlated well with subtraction P.D. (r = 0.74; P is less than 0.001). A subtraction P.D. higher than 26 mV in subjects on a normal sodium intake indicated primary or secondary hyperaldosteronism; if the level was lower than 11 mV four hours after intramuscular injection of 0.25 mg tetracosactrin this suggested mineralocorticoid deficiency. Measurement of oral and rectal P.D. permits rapid and inexpensive diagnosis of aldosterone excess and deficiency. The method may also be used in study of the mineralocorticoid effect of other adrenal steroids: as assessed with this bioassay, the plasma 18-OH-deoxycorticosterone, which is raised in some patients with essential hypertension, lacked any in vivo mineralocorticoid activity.
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PMID:Subtraction potential difference: In-vivo assay for mineralocorticoid activity. 7 36

The renal abnormality which causes hypertension in the Milan hypertensive strain of rats disappears as hypertension develops. Because of the many analogies between the condition in these rats and "essential" hypertension in man, the same pattern of change may occur if a renal abnormality is the cause of essential hypertension in man. This hypothesis was tested in two groups of young normotensive subjects matched for age, sex, and body-surface area; in the first group both parents were hypertensive, and in the second group both parents were normotensive. Renal plasma-flow, glomerular filtration-rate, plasma-volume, plasma-renin activity, plasma-concentrations of Na+, K+, and catecholamines, 24 h urinary excretion of Na+, K+, and aldosterone, and the cardiac index were measured so that renal function and the role of factors affecting blood-pressure regulation could be assessed. Renal plasma-flow was significantly higher (p less than 0.01) in the first group, whereas results of tests for all the other factors were almost the same in both groups. The hypothesis that a primary kidney abnormality causes hypertension in a proportion of patients with essential hypertension is proposed.
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PMID:A renal abnormality as a possible cause of "essential" hypertension. 8 3


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