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

Plasma aldosterone levels were measured during two tests of inhibition in 31 hypertensive patients (13 essential hypertension, 6 bilateral adrenal hyperplasia and 12 documented Conn adenomas) on normal salt diets after withdrawal of all therapy: 1--before and after intravenous infusion of 2 I normal saline in two hours; 2--before and three hours after administration of 1 mg/kg of Captopril. Plasma aldosterone levels greater than 360 pmol/I after salt loading, or greater than 748 pmol/I after Captopril is characteristic of primary tumoral hyperaldosteronism. Apart from the rapidity of the test, Captopril is well-tolerated, does not require acute volume expansion and can be carried out in all forms of hypertension, even in severe cases.
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PMID:[A new diagnostic test for primary tumoral hyperaldosteronism]. 635 34

The diagnosis of primary tumoral hyperaldosteronism is based on a series of hormonal parameters, measured under resting conditions and after stimulation. The results of the administration of a single dose of a converting enzyme inhibitor, Captopril (1 mg/kg body weight per os), can support this diagnosis. In contrast to essential hypertension and hyperaldosteronism due to bilateral adrenal hyperplasia, plasma aldosterone levels remain unchanged in tumoral hyperaldosteronism after administrating Captopril. This is a simple test which can be performed in a morning which clearly differentiated 8 cases of primary tumoral hyperaldosteronism from 6 cases of adrenal hyperplasia.
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PMID:[Primary hyperaldosteronism: diagnostic value of the administration of a single dose of captopril]. 635 35

Following 7 days on a low sodium diet, a regular sodium diet or a high sodium diet each, urine samples were collected from 37 subjects in the final days of each sodium treatment. Urinary kallikrein excretion was determined in 9 patients with primary aldosteronism, 15 normal subjects and 13 patients with essential hypertension. Urinary aldosterone excretion, plasma renin activity (PRA), urinary sodium excretion, urinary potassium excretion and p-aminohippuric acid clearance were also determined on the same days. Levels of urinary kallikrein excretion in patients with primary aldosteronism due to aldosterone-producing adenoma (APA) were greater (p less than 0.05 to p less than 0.001) than those in patients with primary aldosteronism due to idiopathic adrenal hyperplasia (IHA) under any sodium diet. Other examined variables were of limited value in differentiating patients with APA from those with IHA. Urinary kallikrein excretion, urinary excretion of electrolyte, urinary aldosterone excretion, PRA and PAH clearance were similar in normal subjects and patients with essential hypertension. It appears reasonable to conclude from these data that urinary kallikrein does not play an important role in the pathogenesis of essential hypertension, and elevated urinary kallikrein excretion in patients with primary aldosteronism due to APA can be used for biochemical differentiation from those with IHA.
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PMID:Urinary kallikrein excretion in patients with primary aldosteronism: differentiation of adrenal adenoma from idiopathic adrenal hyperplasia. 637 65

Regulation of aldosterone secretion by sodium chloride is impaired in a group of essential hypertensives: high-salt diet fails to suppress aldosterone in these patients despite low renin values. The mechanism of this impaired regulation of aldosterone has not been clarified so far. We tested the sensitivity of aldosterone secretion and blood pressure to A II in 20 normotensive controls (aged 20-60, MAP 92 +/- 3 mm Hg), in ten normotensives with one or two parents with hypertension, and in 21 patients with essential hypertension (aged 17-65, MAP 119 +/- 4 mm Hg). After a period of 6 days on high-salt intake (300-320 mEq Na+/day), A II (0.1, 0.5, 1.0 and 2.0 ng/kg/min) was infused, each concentration for 30 min. According to aldosterone excretion during sodium loading, patients were divided into group A with complete suppression (n = 12, aldosterone excretion 3.6 +/- 0.4 microgram/day) and in group B with insufficient suppression (n = 9, aldosterone excretion 15.5 +/- 2.3 micrograms/day). Despite similarly low plasma renins, rise of serum aldosterone levels during A II infusion was significantly higher in group B patients than in group A patients and normotensive controls. Rise in mean arterial blood pressure, however, brought about by graded A II infusion was similar in both groups of hypertensives and in normotensive controls. The results demonstrate an increased adrenal sensitivity to A II in a subgroup of essential hypertensives only. A similar adrenal hypersensitivity to A II found by others in patients with hyperaldosteronism due to adrenal hyperplasia supports the hypothesis that the same mechanism underlies both disorders.
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PMID:Cardiovascular and adrenal sensitivity to angiotensin II in essential hypertension. 652 58

Dexamethasone suppression adrenal scintiscans were performed on 37 patients referred for evaluation of primary aldosteronism (PA). Twenty-one had aldosterone-secreting adrenal adenoma (AA) and 16 had bilateral adrenal hyperplasia (BAH). The diagnosis of either AA or BAH was confirmed by adrenalectomy in 19 of 21 subjects with AA and by adrenal venous sampling in 15 of 16 patients with BAH. Biochemical parameters of PA were found in each patient while on both high (150 meq Na) and low salt (10 meq Na) intakes. Urinary aldosterone excretion values were 49.7 +/- 10.2 (+/- SEM) micrograms/day (range, 11.2-103.9) and 44.2 +/- 12.1 micrograms/day (range, 14.3-128.0) in AA patients on high and low salt intakes, respectively. In BAH patients, urinary aldosterone values were 29.1 +/- 2.6 micrograms/day (range, 10.0-55.0) and 47.7 +/- 9.0 micrograms/day (range, 23.0-102.0) on high and low salt intakes, respectively. A semioperator-independent computer algorithm was used to calculate adrenal gland uptake of [131I]6 beta-iodomethyl-19-norcholesterol (NP-59) in PA patients and in 7 patients with essential hypertension. NP-59 adrenal uptake values were 0.20 +/- 0.02%/dose (range, 0.03-0.72), 0.28 +/- 0.04% (range, 0.10-0.65), and 0.14 +/- 0.02%/dose (range, 0.08-0.30) in AA, BAH, and essential hypertension, respectively. A significant correlation was found between adrenal gland uptake of NP-59 and urinary aldosterone excretion in AA (r = 0.93; P less than 0.001) and BAH (r = 0.6; P less than 0.01) patients. These data confirm that adrenal gland accumulation of NP-59 while on dexamethasone suppression can be used to characterize abnormal zona glomerulosa function in PA, in addition to localizing AA and differentiating AA from BAH.
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PMID:The relationship of adrenal gland iodomethylnorcholesterol uptake to zona glomerulosa function in primary aldosteronism. 687 87

1. Normokalaemic primary aldosteronism (PA) masquerades as 'essential hypertension', and 50% of patients with aldosterone-producing adenoma (APA) are normokalaemic at presentation to this unit. 2. Angiotensin-responsive (AII-R) APA is as common as angiotensin-unresponsive (AII-U) APA, and requires adrenal venous sampling for differentiation from bilateral adrenal hyperplasia (BAH). 3. From 1981 to 1992, 55 patients with APA underwent unilateral adrenalectomy and were followed up for at least 12 months postoperatively. Hypertension was cured in 55% and improved in the remainder. 4. Cure rate was lower (P < 0.001) in males (11/32, 34%) vs females (19/23, 83%), lower (P < 0.005) in patients over 45 years of age (13/33, 39%) vs those 45 years or younger (17/22, 77%), lower (P < 0.05) in AII-R APA (11/28, 39%) vs AII-U APA (19/27, 70%) and tended to be lower (not significant) in normokalaemic APA (7/17, 41%) vs hypokalaemic APA (23/38, 61%). 5. A higher proportion (P <0.001) of AII-R APA patients were males (23/28, 82%) vs AII-U APA (9/27, 33%), and a higher proportion were from the older age group AII-U APA 13/27, 48%; P < 0.05). Females with AII-U APA who were hypokalaemic had a very high cure rate (16/17, 94%). 6. Since unilateral adrenalectomy cures or improves blood pressure in normokalaemic and AII-R as well as in hypokalaemic and AII-U patients, all hypertensives should be screened for PA, and AII-R APA differentiated from BAH in proven PA.
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PMID:Response to unilateral adrenalectomy for aldosterone-producing adenoma: effect of potassium levels and angiotensin responsiveness. 792 99

The occurrence of hypokalemia in association with high blood pressure is suggestive of primary hypermineralocorticism since in this case both abnormalities might result from a single mechanism. However, adrenal adenomas is well as the various forms of adrenal hyperplasia appear to be quite uncommon, whereas a number of other causes of potassium depletion are far more prevalent and may be associated with essential hypertension. The demonstration of the precise mechanism of both decreased serum potassium and increased blood pressure is a prerequisite for a successful treatment.
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PMID:[Arterial hypertension and hypokalemia]. 823 14

In the last decade, two types of genes participating in the etiology of hypertension have been identified. The primary genes or blood pressure regulators are those that codify enzymes (renin, kallikrein, kininase, aminopeptidase), hormones (angiotensins, vasopressin, aldosterone, prostaglandins, and atrial natriuretic peptide) and substrates (angiotensinogen and kininogen). They cause arteriolar vasodilation or vasoconstriction or sodium retention in the extravascular space. Allelic polymorphisms associated to essential hypertension have been described. The secondary genes are those that produce hereditary diseases of low prevalence, associated to hypertension in 20 to 80% of patients (polycystic kidney disease, pheochromocytoma, adrenal hyperplasia, hereditary nephritis). Forty genes located in all chromosomes, that are dominantly, recessively or X-linked transmitted, have thus far been identified. Chromosomal maps with all genic loci are presented.
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PMID:[The genes of human hypertension]. 946 Feb 75

Low-renin hypertension is common and usually implies increased retention of sodium (Na(+)). In every case of known etiology, there is a mineralocorticoid-induced increase in number of epithelial Na(+) channels (ENaCs) in the collecting duct of the kidney, leading to a state of "hyperENaCactivity." In primary aldosteronism, a result of either an adrenal adenoma or bilateral adrenal hyperplasia, aldosterone itself mediates the increase in ENaC function. A severe form of low-renin hypertension in which a molecular mutation in ENaC prevents removal of the channel from the cell surface, known as Liddle's syndrome, results in increased net ENaC activity but, in this case, independently of an increase in aldosterone. Glucocorticoid remedial aldosteronism, an autosomal dominant form of primary aldosteronism, results from a "new" or chimeric gene for aldosterone synthase. Adrenocorticotropic hormone stimulates its expression as well as secretion of aldosterone. Apparent mineralocorticoid excess results from a molecular mutation that allows cortisol to bind to the mineralocorticoid receptor. Both glucocorticoid remedial aldosteronism and apparent mineralocorticoid excess result in an increase in the number of ENaCs. The question remains whether low-renin essential hypertension is related to an increase in ENaC activity. Low-renin hypertension is most common in black patients, who tend to have lower levels of aldosterone as well as renin, which are features that resemble those found in Liddle's syndrome. Preliminary findings suggest that black patients with low-renin hypertension who are resistant to standard antihypertensive therapy respond favorably to the addition of spironolactone, a mineralocorticoid receptor antagonist that reduces ENaC activity.
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PMID:Low-renin hypertension: more common than we think? 1117 96

Use of the random aldosterone-to-renin ratio (ARR) as a reliable marker of inappropriate aldosterone activity has led to primary aldosteronism (PA) being increasingly diagnosed in hypertensive patients. At least 10% of hypertensives have been found to have PA, the majority of whom presumably have bilateral adrenal hyperplasia or idiopathic hyperaldosteronism as an aetiology for PA. Whilst these patients clearly have excess aldosterone activity, they have in common many features that are found in hypertensive patients in general, amongst which include heightened angiotensin II adrenal sensitivity. Whether these individuals belong within the spectrum of 'essential hypertension' is being debated, but is probably irrelevant clinically since they appear to respond favourably to spironolactone treatment. In addition, there is recent evidence suggesting that these patients overexpress a key enzyme involved in aldosterone production, the aldosterone synthase, the activity of which appears to relate to its genotypic variation.
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PMID:Is aldosterone the missing link in refractory hypertension?: aldosterone-to-renin ratio as a marker of inappropriate aldosterone activity. 1208 Apr 39


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