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

ACTH alpha 1-24 was infused at incremental rates of 12.5-200 mIU/30 min in dexamethasone-suppressed hypertensive patients on a regular sodium diet. The plasma aldosterone response to this stimulus in 8 patients with hyperaldosteronism due to an adrenal aldenoma and 11 with adrenal hyperplasia was significantly greater at all infusion rates (P less than 0.05) when compared with the response in 6 normal subjects on a similar diet. This responsiveness to ACTH in the patients with primary hyperaldosteronism was similar to that of the normal subjects on a low sodium diet. Twelve patients with low renin and 6 patients with normal renin essential hypertension were similarly studied. There was no significant difference in the median aldosterone response between these 2 groups and the normal subjects on a normal diet, but the response was significantly lower compared with that in patients with primary hyperaldosteronism. These data show that patients with hyperaldosteronism from an adrenal adenoma or hyperplasia have a consistent and exaggerated response to ACTH. The hyper-responsiveness is not apparently shared by the majority of patients with low renin essential hypertension and does not support the concept that this group is an intermediate form of primary aldosteronism. Individual patients within this group, however, may have such a response and might be identified by this type of testing.
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PMID:Plasma aldosterone response to ACTH in primary aldosteronism and in patients with low renin hypertension. 22 41

Mineralocorticoids are out of the causes of secondary hypertension. Excess production of mineralocorticoids induces sodium and fluid retention, loss of potassium and metabolic alcalosis. The diagnosis of mineralocorticoid syndromes depends on the interpretation of the functional status of the renin-mineralocorticoid-system, which is in part responsible for the maintenance of normal blood pressure. The classical representative of this group is the syndrome of primary aldosteronism. Causes of mineralocorticoid syndromes associated with hypertension are: 1. autonomous production of mineralo-corticoids by an adrenal adenoma or by idiopathic bilateral adrenal hyperplasia; 2. deficiency of adrenal 17-alpha-hydroxylase or of 11-beta-hydroxylase; 3. secondary aldosteronism associated with primary reninism, or renal arterial stenosis; and 4. pseudo aldosteronism due to excessive ingestion of licorice. Malign or essential hypertension may also often be followed by secondary aldosteronism.
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PMID:[Mineralocorticoid syndromes and hypertension]. 96 85

1. In 7 patients with hypertension, aldosteronism, and low plasma renin (6 patients with a solitary adrenal adenoma, 1 patient with bilateral adrenal hyperplasia) circulatory reflexes (Valsalva's maneuver, head-up tilt and cold pressure test) were examined. Furthermore, the reactivity to the pressor action of tyramine and norepinephrine was determined. For comparison 10 patients with essential hypertension were studied. 2. In 4 of the 7 patients with primary aldosteronism no overshoot following Valsalva's maneuver could be observed. Compared to the patients with essential hypertension the mean overshoot in the patients with primary aldosteronism was significantly reduced. The decrease in blood pressure during head-up tilt was significantly more pronounced in the patients with primary aldosteronism. However, both groups did not differ in their reaction to the cold pressure test. In the patients with primary aldosteronism responsiveness to tyramine was significantly reduced compared to the patients with essential hypertension. No significant difference was observed in the reactivity to norepinephrine between both groups studied. 3. The results point towards a disturbance of the sympathetic nervous system in patients with primary aldosteronism.
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PMID:[Circulatory reflexes in primary aldosteronism (author's transl)]. 121 78

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

We describe four cases of primary hyperaldosteronism whose initial presentation was a moderate to severe hypertension. In three patients an adrenal adenoma was found; in another patient was due to unilateral adrenal hyperplasia. A good therapeutic response was achieved in all cases by unilateral adrenalectomy. The captopril test (Lyons version) proved useful to exclude essential hypertension and, may be, in distinguishing the new sub-types of primary hyperaldosteronism recently described. Indeed, only in the case of unilateral adrenal hyperplasia a fall in plasma aldosterone levels was observed. However, we feel that further investigation is needed to clarify this point.
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PMID:[Significance of the captopril test in the diagnosis of primary hyperaldosteronism --apropos of 4 clinical cases]. 220 22

Plasma concentrations of atrial natriuretic factor and some vasoactive substances were determined in 8 patients with aldosterone-producing adenoma, 10 with idiopathic adrenal hyperplasia, 10 normotensive subjects and 12 patients with essential hypertension. Plasma atrial natriuretic factor concentration in patients with aldosterone-producing adenoma was the highest among the examined groups. Adrenal surgery reduced plasma concentrations of atrial natriuretic factor and aldosterone concomitant with the elevation in urinary sodium excretion, plasma renin activity and urinary sodium-to-potassium ratio. Withdrawal of trilostane (3 beta-hydroxysteroid dehydrogenase inhibitor) in patients with idiopathic adrenal hyperplasia increased plasma concentrations of atrial natriuretic factor and aldosterone, and decreased the urinary sodium-to-potassium ratio, plasma renin activity and urinary sodium excretion. However, reduced urinary sodium excretion following trilostane treatment returned to the control level successively despite the high levels of plasma atrial natriuretic factor and aldosterone. Acute infusion of saline remarkably increased plasma atrial natriuretic factor concentration in patients with idiopathic adrenal hyperplasia and aldosterone-producing adenoma. These results suggest that a high level of atrial natriuretic factor is a characteristic feature in patients with aldosterone-producing adenoma caused chiefly by the expansion of extracellular fluid volume, and circulating atrial natriuretic factor may contribute to regulation of the sodium escape phenomenon in patients with aldosterone-producing adenoma or idiopathic adrenal hyperplasia.
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PMID:The effect of adrenal surgery on plasma atrial natriuretic factor and sodium escape phenomenon in patients with primary aldosteronism. 252 99

In order to evaluate whether changes in the plasma concentration of aldosterone (PA) following the administration of captopril, an inhibitor of angiotensin-converting enzyme, will establish the diagnosis of primary aldosteronism we have used this test in 9 healthy subjects and in 22 patients with various forms of hypertension, including 5 patients with primary aldosteronism due to idiopathic adrenal hyperplasia (n = 4) or aldosterone-producing adenoma (n = 1). The response of PA to captopril (25 mg orally) was investigated on an outpatient basis, following a rest period of 120 minutes in the supine position. In healthy subjects PA decreased from a mean basal value of 11.5 +/- 5.9 ng/dl to less than 6.4 ng/dl (4.9 +/- 1.4 ng/dl [p less than 0.01]). Similarly, captopril induced a fall in PA concentration to less than 6.4 ng/dl in patients with essential hypertension, with renal artery stenosis or with an afunctional kidney. Post-captopril concentrations of plasma aldosterone were about twice the normal level in 3 of 4 patients with idiopathic adrenal hyperplasia and about four-fold raised above normal in the patient with an aldosterone-producing adenoma. In spite of a false-negative result in one patient with idiopathic adrenal hyperplasia, the administration of captopril appears to be of use in recognizing patients with primary aldosteronism on an outpatient basis.
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PMID:[Detection of primary aldosteronism using the captopril test]. 331 69

Of 15 patients with primary aldosteronism, 7 had idiopathic adrenal hyperplasia (IHA) and 8 had aldosterone-producing adenoma (APA). In order to determine any renal problems involved in the treatment, the renal clearance of these patients was analyzed and the results compared with those obtained from 12 patients with essential hypertension. With water diuresis or under antidiuresis status, levels of urine volume, Cosm and CH2O in patients with APA were greater (p less than 0.05-p less than 0.001) than those of patients with essential hypertension, while the fractional tubular sodium delivery of the former patients was lower than that of the latter patients (p less than 0.001 or less than 0.05). A similar tendency was observed in clearance studies in patients with IHA, although to a lesser extent. Adrenal surgery for patients with APA normalized these values, but administration of trilostane (3 beta-hydrosteroid dehydrogenase inhibitor) to patients with IHA failed to improve these values. These results indicate that impaired urinary concentrating ability as well as reduced urinary diluting capability is a common feature of primary aldosteronism. Such impaired renal function was improved only in patients with APA after adrenal surgery.
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PMID:Evidence for a defect in urinary concentrating ability in primary aldosteronism and its reversal by adrenal surgery. 367 60

Serum 18-hydroxycorticosterone, aldosterone, and potassium were measured under basal conditions in 34 patients with documented primary aldosteronism, 10 patients with essential hypertension, and 9 normal subjects. The results revealed that 22 of 23 patients with aldosterone-producing adenomas had 18-hydroxycorticosterone levels greater than 100 ng/dl, and all 9 patients with idiopathic adrenal hyperplasia had plasma levels less than 100 ng/dl. Two patients with unusual macromicronodular hyperplasia of the adrenal glands had levels greater than 100 ng/dl. We found a significant relationship between serum potassium and the ratio of 18-hydroxycorticosterone to aldosterone in patients with idiopathic adrenal hyperplasia, but not in those with an aldosterone-producing adenoma. We conclude that measurement of serum 18-hydroxycorticosterone is a useful predictor of the etiology of primary aldosteronism.
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PMID:The prediction of anatomical morphology of primary aldosteronism using serum 18-hydroxycorticosterone levels. 396 94

Plasma aldosterone levels were measured as part of two suppression tests in 31 hypertensive patients on normal sodium diet and without recent treatment. Thirteen patients had essential hypertension, 6 had probable bilateral adrenal hyperplasia and 12 had confirmed Conn's adenoma. In the first test, aldosterone levels were measured in the supine patients, then after infusion of 2 litres of isotonic saline over 2 hours. In the second test, aldosterone levels were measured before and 3 hours after oral administration of Captopril 1 mg/kg. Plasma aldosterone values superior to 360 pmol.l-1 after sodium load or to 665 pmol.l-1 after Captopril were characteristic of primary hyperaldosteronism due to adenoma. The test using Captopril has the advantages of being rapid, of avoiding acute blood volume expansion and of being applicable to all forms of hypertension, including severe ones.
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PMID:[A simple diagnostic test for primary hyperaldosteronism]. 622 41


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