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

The hypothesis that hyperaldosteronism is not the sole cause of hypertension in dexamethasone-suppressible hyperaldosteronsim was tested in an 18-year-old male. After six years of little or no treatment, the hypertension and mild hyperaldosteronism were promptly decreased by a small dose of dexamethasone. During dexamethasone treatment, when aldosterone secretion was suppressed to less than normal and he was normotensive, steroids were given by constant infusion in an attempt to reproduce the hypertension of the dexamethasone-free state. Neither five days of aldosterone or 18-hydroxydesoxycorticosterone (18-OH-DOC) at 1 mg/day, nor desoxycorticosterone (DOC) at 30 mg/day caused hypertension. However, sodium retention and potassium loss was observed during aldosterone and DOC infusion. Hypertension was produced within five days during infusion with ACTH or oral metyrapone. The hypertensive effect of the latter was abolished by addition of aminoglutethimide treatment. These studies suggest that a steroid other than aldosterone, 18-OH-DOC, or DOC may be the cause of the ACTH-induced hypertension in this patient. The aminoglutethimide data suggest that the ACTH effect on blood pressure is due to a steroid, and the metyrapone studies suggest that the steroid may be an 11-desoxysteroid. Urine and blood collected under ACTH stimulation and metyrapone treatment may be a rich source from which we may characterize this hormone.
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PMID:Evidence for an unidentified ACTH-induced steroid hormone causing hypertension. 18 12

A study was made of 77 patients with adiposity and a group of healthy persons with normal weight. Patients with adiposity had a significant increase of blood plasma aldosterone level; of decisive role in the formation of secondary hyperaldosteronism was played by the elevation of blood renin level. Apparently activation of the renin-angiotensin system and the associated intensification of mineralocorticoid function of the adrenal glands served as one of the causes of development of arterial hypertension in persons with excessive weight. In adiposity there proved to be an increased rate of cortizol secretion and of 17-OCS excretion with the urine; as to the blood plasma cortizol concentration, it failed to show any significant difference from the normal. Apparently stable blood cortizol level in the patients with adiposity was maintained as a result of intensified ACTH secretion; in these patients reserve possibilities of the adrenocorticosteroid function of the hypophysis were diminished.
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PMID:[Mineralocorticoid and glucocorticoid functions of the adrenal cortex and some mechanisms of their regulation in obesity]. 19 62

Primary hyperaldosteronism usually causes moderate hypertension. It is rare to note as in our two patients intermittent attacks of paroxysmal hypertension. The diagnosis of aldosteronism will be suspected on the finding of persistent hypokalemia with acidosis. It will be confirmed by laboratory examinations severe fall in plasma renin activity and rise in aldosterone in the adrenal veins. To determine the affected side, one may carry out adrenal phlebography which is a difficult technic, and/or a scan using iodine cholesterol which is benign and precise. Surgery with removal of the adenomatous hyperplasia in one case and of an adenoma in the other, gave one very good result.
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PMID:[Primary hyperaldosteronism with paroxysmal arterial hypertension. Apropos of 2 operated cases]. 20 43

Hypertension in 17 alpha-hydroxylase deficiency was studied by comparing it with hypertension in Cushing syndrome or that in primary aldosteronism. Furthermore, the role of endogenous increases of ACTH, deoxycorticosterone, and 18 alpha-hydroxy-deoxycorticosterone upon blood pressure was studied in rats by administerating metopirone. Hypertension in 17 alpha-hydroxylase deficiency was considered to be more similar to that in primary aldosteronism from the studies on renin components, pressor responses to angiotensin II and norepinephrine, and renin responses to stimulations. Plasma catecholamines were slightly decreased in 17 alpha-hydroxylase deficiency. The hypertension was alleviated by the administeration of dexamethasone in 2 of 3 patients with 17 alpha-hydroxylase deficiency. However, in the remaining one who had an accelerated hypertension and normal renin, the hypertension was not alleviated by dexamethasone. In the animal studies, hypertension induced by metopirone was accelerated by salt loading of uni-lateral nephrectomy plus salt loading. In those rats, plasma ACTH, and deoxycorticosterone were markedly increased.
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PMID:Hypertension induced by adrenocortical dysfunction--hypertension in 17 alpha-hydroxylase deficiency and metopirone-induced hypertension. 21 19

Urinary Prostaglandin E2 (PGE2), a known indicator of renal production, was measured by specific radioimmunoassay in 111 normal volunteers, 85 patients with essential hypertension, 6 with renovascular hypertension, and 23 patients with primary aldosteronism. Women excreted less PGE2 than men in both normotensive and hypertensive groups. When compared to normals, essential hypertensives demonstrated significantly lower PGE2 levels, with one third excreting less than 100 ng/24 hr, values usually seen only in subjects receiving the prostaglandin synthetase inhibitor, indomethacin. Normal PGE2 was seen in patients with renovascular hypertension, and levels were uninfluenced by treatment with the converting enzyme inhibitor SQ14225, Despite normalization of blood pressure and increased plasma renin activity. Normal PGE2 was also encountered in primary aldosteronism. These data indicate that impaired renal PGE2 biosynthesis is specific for human essential hypertension, and is not secondary to the elevated blood pressure. Although PGE2 excretion tends to be lower in low-renin hypertension, a constant relationship between PGE2 and renin is not always apparent.
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PMID:Impaired renal prostaglandin E2 biosynthesis in human hypertensive states. 21 95

The effect of a 5 day ACTH test (40 U/24 h) on plasma aldosterone (aldo), deoxycorticosterone (DOC), plasma renin activity (PRA) and urinary excretion of aldosterone-pH1-conjugate (pH-1-aldo) and tetrahydro-DOC (TH-DOC) was investigated in 8 normotensive children (group I), 8 patients with hypertension of unknown origin (group II), and 4 hypertensive children with dexamethasone suppressible hyperaldosteronism (DSH) (group III). Changes in blood pressure and sodium balance were studied in all groups. Under baseline conditions there was no hormonal difference between group I and II. In contrast, the children in group III had a suppressed PRA and a 1.5--2 fold elevation of aldo and DOC. Plasma DOC and urinary THDOC increased continuously 10--50 fold in all groups during the ACTH test. Aldo rose transiently 2--4 fold on the first day of ACTH and fell subsequently below baseline levels in group I and II. The children with DSH (group III), however, showed an unusual, sustained aldo stimulation with ACTH. PRA decreased significantly after ACTH in group I and II. Sodium retention aTH administration. The highest blood pressure rise was observed in group III (from 124/72 to 139/90 mm Hg). The blood pressure response to ACTH was partly sodium dependent. Although aldo and DOC and sodium retention may contribute to the ACTH induced blood pressure elevation, other factors must play a role.
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PMID:Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension. 21 19

Neurohumoral mechanisms operating via the catecholamines are discussed in their relationship to such hypertensive diseases as pheochromocytoma and labile and established essential hypertension. 2. In pheochromocytoma, diagnosis depends almost entirely on identification of increased amounts of catecholamine metabolites in the urine. Because of the danger, manipulative or invasive procedures both for diagnosis and during surgery should be kept at a minimum. 3. In established essential hypertension, reactivity to norepinephrine and plasma norepinephrine are increased, whereas norepinephrine uptake and apparent secretion rate are decreased. 4. In labile essential hypertension, reactivity to epinephrine and probably plasma epinephrine are increased and uptake of epinephrine decreased. 5. Labile hypertension with all its characteristics may or may not coexist with established essential hypertension with all its features. 6. The sympathetic nervous system is also involved in other types of hypertensive disease. Many patients with renovascular hypertension as well as with primary and secondary hyperaldosteronism also have essential hypertension. Angiotensin II affects the sympathetic nervous system and the juxtaglomerular apparatus appears to be beta adrenergic receptor activated, at least in part.
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PMID:Neurohumoral mechanisms in hypertension. 23 64

Rectal potential difference (pd) is directly related to the plasma aldosterone concentration, and rises when aldosterone is stimulated by sodium deprivation. However, when the measurement of rectal pd was tested at a screening test for hyperaldosteronism in 19 hypertensive subjects, four of the eight with primary hyperaldosteronism had a normal pd and four of the eight without aldosterone excess had an abnormally raised potential difference. The technique cannot therefore be recommended as a routine screening test for hyperaldosteronism. No relationship was found between rectal pd and hypertension associated with excess of deoxycorticosterone. Rectal pd rises in response to the mineralocorticoid-like agent carbenoxolone.
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PMID:Rectal potential difference in the diagnosis of aldosterone excess. 23 2

An 18-year-old female was found to be hypertensive on routine medical examination. Further investigation disclosed persistent hypokalaemia and elevated plasma renin activity in peripheral venous blood. Segmental renal vein sampling with assay of blood samples located the source of excess renin secretion in the lower mid-zone of the left kidney. This localization was not confirmed by either angiography or by palpation of the exposed kidney before nephrectomy but macroscopic examination of the freshly sectioned kidney revealed a small tumour in the region suggested by renal vein sampling. The tumour had the morphologic pattern fo an haemangiopericytoma with abundant ultrastructural specific granules and very high renin activity by tissue assay. Plasma renin activity fell precipitously after nephrectomy and remained very low for the first week. Although the immediate post-operative blood pressure fell to normal, hypertension recurred temporarily and was associated with elevated plasma aldosteron, producing a syndrome similar to primary aldosteronism. All variables returned to normal without specific therapy and hypertension has not subsequently recurred.
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PMID:Hypertension due to a renin-secreting tumour localised by segmental renal vein sampling. 27 40

1. Noradrenaline and adrenaline in the adrenal vein of essential hypertensive patients are almost exclusively (99%) unconjugated or free. However only 17% of dopamine is free, the rest is conjugated. The further the site of sampling from the adrenal vein the closer come the free catecholamines to their normal peripheral venous proportion (noradrenaline + adrenaline 20%, dopamine less than 1% of total catecholamines). Deviations from these patterns help to detect the site and type of secretion of phaeochromocytoma. 2. Essential hypertensive patients have, compared with control subjects, higher conjugated plasma dopamine, less urinary free and conjugated dopamine with blunted urinary free dopamine and sodium responsiveness to frusemide. Conjugated noradrenaline + adrenaline, mean arterial pressure and age are positively interrelated. 3. Patients with primary aldosteronism have elevated plasma and urinary total dopamine. After removal of the adenoma urinary dopamine excretion decreases to normal. 4. Elevated conjugated dopamine appears to reflect a compensatory activation of the dopaminergic vasodilator pathway in hypertension, the total urinary dopamine excretion an intrinsic deficiency or compensatory increase of a dopamine-modulated natriuretic mechanism.
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PMID:Free and conjugated catecholamines in human hypertension. 28 3


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