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

Among the forms of endocrine hypertension, attention has recently been turned, apart from pheochromocytoma, to hypertensions caused by overproduction of mineralocorticoids. In this category are included, in addition to the classic Conn syndrome, aldosteronism associated with bilateral adrenal hypertrophy, dexamethasone-suppressible aldosteronism, and overproduction of mineralocorticoids (other than aldosterone) in the case of defects in the steroidogenesis enzyme system. In these cases, mineralocorticoid overproduction is accompanied by a low level of renin, by hypokalemic alkalosis. Secondary hyperaldosteronism, due to the stimulation of aldosterone secretion by increased activity of the renin-angiotension system, occurs during the malignant phase and in cases of renovascular hypertension. Estrogens, in cyclically secreted physiological quantities, have rather a protective effect on the origination of hypertension. At high dosages (as in contraceptives), estrogens can induce or aggravate hypertension in susceptible women by their effect on the activity of the renin-angiotensin-aldosterone system, notably by increasing the renin substrate. In the case of essential hypertension, deviations were found in the functioning of catecholamine storage granules in the sympathetic nerve endings. The renin-angiotensin-aldosterone system functions as an accelerating factor only in the advanced phase of essential hypertension, and the possibility of its participation in development of malignancy cannot be eliminated. A special group is comprised of essential hypertension with renin suppression, which is associated with a relatively high level of urinary excretion of dopamine as compared with noradrenalin. In renovascular hypertension, the renin-angiotensin-aldosterone system most often functions as an etiopathogenetic factor at the onset of the disease. In advanced stages, increased blood pressure levels must be considered to be attributable to other factors. Blood pressure regulati on and idiopathogenesis in hypertension cases are complex processes induced by the interaction of several different hemodynamic, nervous, and humoral factors. The study of humoral factors contributes to etiopathogenetic understanding and to the differential diagnosis of the various kinds of hypertension.
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PMID:[New data on hormone-dependent hypertension and their significance for the practice]. 434 13

Fecal and salivary sodium and potassium concentrations were measured in 22 hypertensive patients with hypokalemia who were undergoing investigation for primary aldosteronism due to an adrenocortical adenoma (Conn's syndrome). Of eight patients with a high aldosterone secretion rate, five had clearly low fecal Na/K ratios, (including all four patients with Conn's syndrome), in three the ratios were equivocal. Of 14 patients with hypertension and a normal aldosterone secretion rate, none had a sufficiently low fecal Na/K ratio strongly to suggest hyperaldosteronism, although two were borderline. Salivary electrolyte concentrations were not as consistent an indicator of mineralocorticoid hormone excess. Estimation of fecal sodium and potassium concentrations may be useful in the diagnosis of mineralocorticoid hormone excess and in assessing the results of therapy.
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PMID:Fecal and salivary electrolytes in the diagnosis of primary aldosteronism. 515 Mar 32

The etiology of several specific types of hypertension are described in order of increasing difficulty of diagnosis: glycyrrhizine poisoning, oral contraceptives, coarctation of the aorta, pheochromocytoma, Conn syndrone, Cushing syndrome, parenchymal nephropathy, unilateral renal atrophy, and renovascular hypertension. Glycerryyzine and oral contraceptive etiologies can be diagnosed by questioning the patient and improved by eliminating their intake. Coarctation of the aorta is easily identified by clinical signs, but surgical repair is probably mor e risky than drug treatment. A pheochromocytoma is signaled clinically and by catecholamine excretion. Conn syndrome has characteristic clinical signs, particularly hypokalemia during intake of diuretics. Cushing syndrome is recognized by corticosteroid excretion as well as peculiear obesity, acne, erythrosis, and diabetes. Bilateral nephropathy is common (25% of hypertensions) and rather difficult to dia gnose and treat. Unilateral renal atrophy can be demonstated by renal arteriography and cystography, but predicting the outcome of nephrectomy is problematic. Renovascular hypertension due to occlusion of the renal artery requires the most sophisticated tests and care for an effective treatment. A table and an outline of diagnostic tests to differentiate these disorders are included.
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PMID:[Etiologic survey of arterial hypertension. Its justifications and practical modalities]. 549 42

Adrenal cortical adenomas with diameters greater than 3 mm. were found in 185 (3.61%, of 5,120 consecutive necropsies. A progressively higher incidence with increasing age was noted) 82% of the adenomas occurring in cases in the age range 51-80 years. On the basis of age distribution of adenomas and their connexion with hypertension, there does not seem to be sufficient proof to suppose that the cortical adenomas frequently found at necropsy can be held responsible for causing normokalaemic primary aldosteronism to the extent assumed by Conn (1964).
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PMID:Possibility of normokalaemic primary aldosteronism as reflected in the frequency of adrenal cortical adenomas. 601 87

The adrenal cortex is an important factor in the control of electrolyte and water balance and in blood pressure homeostasis. Not surprisingly, therefore, hyper- and hyposecretion of one or more of its products has extensive repercussions. Hypersecretion of aldosterone, as seen in primary hyperaldosteronism and related diseases, and of other mineralocorticoids such as corticosterone and/or 11-deoxycorticosterone, as seen in 17 alpha-hydroxylase deficiency or 11 beta-hydroxylase deficiency syndromes, respectively, are associated with hypertension, sodium retention, potassium wastage and a metabolic alkalosis. On the other hand, impaired secretion, as in Addison's disease or in congenital deficiencies of other steroid-synthesizing enzymes, leads to hypotension, sodium loss with hypovolaemia, and hyperkalaemia. In each case, these disturbances of electrolyte metabolism may cause neurological and muscle dysfunction. The relationship between glucocorticoid hypertension and electrolyte metabolism is less clear and the importance of the adrenal cortex in the aetiology of essential hypertension is still being assessed.
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PMID:Disorders of the adrenal cortex: their effects on electrolyte metabolism. 609 53

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

The humoral and hemodynamic effects of converting enzyme inhibition captopril are presented in two patients with primary hyperaldosteronism (PHA). In all, 20 patients with resistant hypertension were treated with the angiotensin converting enzyme inhibitor captopril. In 18 patients with essential or renovascular hypertension mean (+/- SEM) plasma renin activity (PRA) rose from 5.0 +/- 1.4 to 35.3 +/- 5.3 ng/ml/hr (P less than 0.01) and mean (+/- SEM) plasma aldosterone (PA) declined from 25.8 +/- 2.9 to 15.1 +/- 1.9 ng/ml (P less than 0.01) after captopril. In two patients with PHA the PRA was not stimulated by converting enzyme inhibition, although there was modest decline in PA and a temporary reduction in blood pressure. After surgical removal of aldosterone-producing adenomas, PRA responsed appropriately to captopril. These cases illustrate that a disease process can modify the response to a drug and demonstrate that, in patients with PHA, captopril does not stimulate PRA, induces only minor decrements in PA, and is relatively ineffective as an antihypertensive.
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PMID:Converting enzyme inhibition with captopril in patients with primary hyperaldosteronism. 627 45

Ten patients with primary hyperaldosteronism resulting from a functioning adrenocortical adenoma were studied. The high incidence of hypertension and/or renal disease in the families of these patients suggests that hereditary factors play a part in the genesis of aldosteronomas. In patients with hypertension and hypokalemia the diagnosis of primary hyperaldosteronism is established by measurements of serum renin activity and serum aldosterone concentrations under normal conditions and during pharmacodynamic tests. The adenoma is demonstrated by radioactive iodocholesterol scintigraphy and computerized tomography. In nearly two-thirds of the patients, unilateral adrenalectomy is followed by complete definitive recovery.
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PMID:[A review of ten cases of aldosteronoma. Diagnostic and therapeutic conclusions (author's transl)]. 628 23

We present the first report of primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. A 10-year-old white boy with severe hypertension (150/100 mm Hg), hypokalemia (1.4 mEq/liter), and suppressed plasma renin activity (PRA) (less than 0.1 ng/ml/hr) demonstrated fixed PRA and aldosterone (aldo) levels that did not change with alteration of dietary sodium. The paradoxical decrease in serum aldo on assumption of upright posture suggested a tumor. Prolonged ACTH administration produced a continuous rise in blood pressure, but a transient rise in aldo. A minimal decrease in urinary aldo during dexamethasone administration was noted, excluding dexamethasone-suppressible hyperaldosteronism. Blood pressure normalized with spironolactone. Computerized transaxial tomography, iodocholesterol scanning, and adrenal venography were not diagnostic of a discrete adrenal lesion. Although hyperplasia is more common than an adenoma as a cause of hyperaldosteronism in childhood, a tumor was predicted, since adrenal vein hormone sampling with ACTH stimulation lateralized aldosterone secretion unequivocally to the left adrenal gland. However, left adrenalectomy revealed macronodular hyperplasia. Postoperatively, there was reversal of hypertension, hypokalemia, and hyperaldosteronism. Thus, in childhood, unilateral hypersecretion of aldosterone may result from nodular hyperplasia, rather than a discrete adenoma.
Hypertension
PMID:Primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. Case report. 631 81

Two patients with both primary hyperparathyroidism and primary hyperaldosteronism are described. Each presented with high blood pressure and a history of renal calculi. Mild hypercalcaemia was associated with raised plasma parathyroid hormone concentrations and a parathyroid adenoma was excised from each. Both patients also had hypokalaemia, hyperaldosteronism and low plasma renin concentrations. Quadric analysis, adrenal vein plasma aldosterone concentrations, adrenal venography and CT scanning all suggested an adrenal adenoma in each patient. This suspicion was confirmed at operation in one patient; the other patient is unfit for adrenal surgery but her blood pressure and plasma potassium concentration have remained within the normal range during prolonged treatment with either spironolactone or amiloride. Because of this unusual association a search was made for parathyroid hormone excess in patients with primary hyperaldosteronism and for aldosterone excess in primary hyperparathyroidism. None was found.
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PMID:Primary hyperparathyroidism associated with primary hyperaldosteronism. 634 7


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