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Query: UMLS:C0020538 (hypertension)
 170,190 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

In 3 patients with longstanding hypertension and spontaneous or diuretic-induced hypokalemia, the diagnosis of primary aldosteronism was established by the dual criteria of non-suppressible plasma aldosterone level and suppressed plasma renin activity. Preoperative studies of the etiology for the hyperaldosteronism using the postural plasma aldosterone test and adrenal venous steroid measurements gave conflicting results. On the basis of the differential adrenal venous steroid content, which suggested an unilateral adrenal source for the aldosterone hypersecretion, presumed to be adrenal adenoma, each patient was operated upon. In each case the excised adrenal revealed adenomatous or macronodular hyperplasia. Reinvestigation of the patients 3 to 12 months after the adrenalectomy showed that the dynamics of the renin-aldosterone axis was now restored to the normal state even though the patients remained hypertensive. These findings indicate that unilateral hypersecretion of aldosterone associated with adrenal hyperplasia can occur in some patients with primary aldosteronism simulating that due to an aldosteronoma. Such observations also raise questions about the pathogenesis of the adrenal hyperplasia and seem to add further complexity to the evaluation of patients with hyperaldosteronism.
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PMID:Unilateral hypersecretion of aldosterone associated with adrenal hyperplasia as a cause of primary aldosteronism. 636 63

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

Primary aldosteronism due to primary adrenal hyperplasia (PAH) is described. Hypertension, hypokalaemia, hyperaldosteronism and renin suppression were corrected by unilateral adrenalectomy in 3/5 patients and by spironolactone treatment in 2/5. Blood pressure and hormonal parameters have remained normal for up to seven years after surgery and spironolactone management. Four patients had bilateral micro- and macronodular hyperplasia and one had unilateral hyperplasia. While hormonally and biochemically identical to patients with aldosterone producing adenoma, PAH can be distinguished from idiopathic hyperaldosteronism (adrenal hyperplasia). The inability to demonstrate a tumour by computed tomography but the presence of bilateral elevations of aldosterone concentration in adrenal venous blood identifies PAH.
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PMID:Primary aldosteronism is comprised of primary adrenal hyperplasia and adenoma. 659 73

The existence of a new subset of primary hyperaldosteronism that combines the morphology of bilateral hyperplasia with the biochemical and therapeutic responses typical of adenoma recently was suggested. The following is the first detailed case report of that subset. The patient had severe hypokalemia and hypertension responsive to spironolactone, and elevated supine plasma aldosterone and 18-hydroxycorticosterone values that did not increase after ambulation. Surgical removal of 75% of both adrenal glands decreased mineralocorticoid levels into the low normal range and allowed the return of normal renin-angiotensin function, although plasma aldosterone was still unresponsive to postural change. Glucocorticoid reserve remained normal. Histology showed bilateral cortical hyperplasia. The results support the existence of a new subset of adrenal hyperplasia, termed primary adrenal hyperplasia, in which biochemical parameters and response to surgery mimic those of adrenal adenomas. The existence of such a subset indicates that morphological categorization alone is insufficient to rule out a possible therapeutic response to surgery in patients with aldosterone-secreting adrenal hyperplasia.
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PMID:Primary adrenal hyperplasia: a new subset of primary hyperaldosteronism. 670 84

Amiloride is a potassium-sparing diuretic used in spontaneous and diuretic-induced hypokalemia. The effect of amiloride was studied prospectively in 12 patients with primary hyperaldosteronism. Four patients had unilateral adrenal adenomas and eight had bilateral adrenal hyperplasia. All patients were hypertensive and their mean plasma potassium levels were low. Amiloride, 10 to 40 mg daily, was given for 6 mo. Mean plasma potassium levels rose (0.96 mEq/l, P less than 0.001) and remained normal throughout the study without potassium supplementation. Mean blood pressure was lowered by amiloride (22/10 mm Hg, P less than 0.001) but normotension required concomitant antihypertensive therapy in most patients. No significant adverse clinical or laboratory experiences could be directly attributed to amiloride therapy. There was no correlation between the response to therapy and the plasma aldosterone levels, aldosterone secretion rate, or presence of a unilateral adrenal adenoma. Our study demonstrates the efficacy of amiloride in the correction of hypokalemia and amelioration of hypertension in primary hyperaldosteronism.
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PMID:Amiloride in primary hyperaldosteronism. 705 5

Parenteral administration of progesterone in normal man provokes an increased sodium and chloride urinary secretion during the 1st days of treatment with no change in kaliuresis. This effect is antagonist to aldosterone. Like spironolactone, progesterone competes with the mineralcorticoid cytoplasmic receptor of renal distal tubular cells. The lack of net variation of kaliuresis under progesterone remains however ill understood. In the healthy subject progesterone-induced natriuresis stimulates plasma renin activity and secondary aldosteronism restricts the amplitude of total sodium loss. Progesterone action may therefore account for the stimulation of the angiotensin renin system during the luteal phase of the menstrual cycle and also contribute to the increased aldosterone secretion during pregnancy. Its pathogenetic role in premenstrual edema is controversial. 17-hydroxyprogesterone which is secreted in large amounts during adrenal hyperplasia due to a block of 21 hydroxylase, has a natriuretic action comparable to that of progesterone, which accounts for the constant activation of the renin system in that condition. Synthetic progestatives do not have the natriuretic action of progesterone; their affinity for the renal tubular receptor in vitro is very small or nil. They do not, however, seem to account for the arterial hypertension observable with the estroprogestative pill. They should be used with care in the woman with hypertension. On the other hand, oral contraception with continuous minimal doses of progestatives seem quite well tolerated with regard to blood pressure. (author's modified)
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PMID:[Progesterone, progestatins and water and sodium metabolism]. 723 20

Two siblings with congenital Cushing's syndrome due to bilateral nodular adrenal hyperplasia are described. The older, a boy, presented with severe hypertension and died soon after subtotal adrenalectomy. His sister, who had clitoral enlargement and showed persistent hyponatraemia, had a two-stage total adrenalectomy and is still alive. Investigations in the second case showed grossly elevated urinary cortisol metabolites, 17-oxosteroids and 3 beta-hydroxy-5-ene-steroids. These were not suppressed by dexamethasone, and plasma ACTH was undetectable, indicating that the disorder was not due to excessive ACTH secretion. Cell culture studies on the resected adrenals failed to demonstrate an abnormal pattern of steroid synthesis in vitro, and normal trophic responses were obtained with 1-24 ACTH and monobutyryl cyclic AMP. No stimulation of steroid synthesis was obtained with a range of polypeptide hormones, and the cause of the adrenal hyperplasia remains unknown.
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PMID:Familial congenital Cushing's syndrome due to bilateral nodular adrenal hyperplasia. 730 79

Techniques for pro-operative localization of aldosterone-secreting adrenal adenomas were studied in thirty-seven patients, each with hypertension and biochemical evidence of primary hyperaldosteronism and each later having adrenal surgery (thirty-two adenomas, five bilateral hyperplasia). Bilateral adrenal vein catheterization was attempted in all cases; it was successful on the left side in all patients and in 92% of cases on the right. Adrenal vein plasma samples were obtained from the left side in 92% and from the right in 73% of cases. Adrenal vein plasma aldosterone measurements correctly indicated the presence of tumour in twenty-eight cases but falsely predicted unilateral adenoma in two cases of bilateral adrenal hyperplasia. Adrenal venography also correctly predicted unilateral adrenal adenomas in twenty-six cases but falsely suggested the presence of tumour in three cases of bilateral adrenal hyperplasia. Computed tomography (CT) was used in the last eight cases. In seven instances the predictions (six adenomas, one bilateral adrenal hyperplasia) were confirmed at surgery. However, the remaining patient harboured an adenoma 20 mm in diameter which was not detected by CT although diagnosed both by adrenal venography and adrenal vein aldosterone measurements. Ultrasound detected adenoma in only three of twenty-two cases examined. Although further comparative studies of the type described here are required, the results of computed tomography are promising and suggest that this non-invasive technique might well become the first choice procedure in localizing aldosterone-secreting adenomas.
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PMID:Pre-operative localization of aldosterone-secreting adrenal adenomas. 732 51

Glucocorticoid-suppressible hyperaldosteronism is a dominantly inherited form of hypertension believed to be caused by the presence of a hybrid CYP11B1/CYP11B2 gene which has arisen from an unequal crossing over between the two CYP11B genes in a previous meiosis. We have studied a French pedigree with seven affected individuals in which two affected individuals also have adrenal tumors and two others have micronodular adrenal hyperplasia. One of the adrenal tumors and the surrounding adrenal tissue has been removed, giving a rare opportunity to study the regulation and action of the hybrid gene causing the disease. The hybrid CYP11B gene was demonstrated to be expressed at higher levels than either CYP11B1 or CYP11B2 in the cortex of the adrenal by RT-PCR and Northern blot analysis. In situ hybridization showed that both CYP11B1 and the hybrid gene were expressed in all three zones of the cortex. In cell culture experiments hybrid gene expression was stimulated by ACTH leading to increased production of aldosterone and the hybrid steroids characteristic of glucocorticoid-suppressible hyperaldosteronism. The genetic basis of the adrenal pathologies in this family is not known but may be related to the duplication causing the hyperaldosteronism.
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PMID:Glucocorticoid-suppressible hyperaldosteronism and adrenal tumors occurring in a single French pedigree. 759 10


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