Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031511 (pheochromocytoma)
 14,622 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular and plasma catecholamine responses to metoclopramide (MCP), a dopamine antagonist, were examined in 5 patients with pheochromocytoma, 12 patients with essential hypertension (EHT) and 9 normotensive (NT) subjects who displayed symptoms suggestive of pheochromocytoma on a constant daily intake of 100 mEq sodium and 80 mEq potassium. Significant pressor responses to intravenous doses of 5 mg of MCP, which produced no serious pressor episodes and no other undesirable side effects, were found only in the patients with pheochromocytoma, in contrast to the subjects with EHT and NT who tended to display slight depressor responses. After curative surgery for pheochromocytoma, the MCP-induced pressor effects returned to normal. Furthermore, the enhanced pressor effects of MCP in the patients with pheochromocytoma were associated with increased plasma norepinephrine (NE) concentrations. However, the plasma epinephrine (E) concentrations remained unchanged after the MCP injection. Thus, this dose of MCP appears to be a more suitable vasopressor provocative agent in the pharmacological diagnosis of pheochromocytoma compared to currently used agents.
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PMID:Metoclopramide in the diagnosis of pheochromocytoma. 405 55

Dihydroxyphenylglycol (DOPEG) is a metabolite of noradrenaline (NA) in the sympathetic nerve endings, and dihydroxymandelic acid (DOMA) is one in the extraneuronal tissues. The measurement of plasma DOPEG and DOMA were evaluated with NA as one of the clinical indices of sympathetic nerve activity. These were measured in essential hypertension and also applied for diagnosis of pheochromocytoma. Plasma DOPEG levels were correlated with NA. Plasma NA and DOPEG were decreased after oral administration of clonidine (150 micrograms) and plasma DOPEG levels were slowly increased after standing. Therefore, plasma DOPEG seemed to be useful as one of the rather stable indices of the sympathetic nerve activity. Plasma NA and DOPEG levels in WHO stage I essential hypertension were higher than those in normotensive controls. Observed normal plasma noradrenaline and DOPEG levels in stage II reflect the normalized sympathetic tone in this stage. The elevation of plasma NA and DOMA levels in stage III seemed to be at least partly explained by renal function disturbance. In patients with pheochromocytoma, despite of the marked elevation of plasma NA and DOMA, plasma DOPEG showed only three-fold elevation and the ratio DOPEG/NA was reduced. The simultaneous measurement of plasma NA, DOPEG and DOMA is useful to evaluate sympathetic nerve activity in essential hypertension and to differentiate pheochromocytoma in hypertension.
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PMID:Plasma noradrenaline and its deaminated metabolites in essential hypertension and pheochromocytoma. 406 1

The present study was performed to investigate whether or not there were enkephalins in plasma and urine in normal subjects and in patients with various diseases. Two kinds of antisera were developed to detect M-enk and L-enk. One has specific affinity with the C-terminus of methionine-enkephalin sulfoxide (M-O-enk), the oxidized form of M-enk, and the other with the N-terminus of L-enk. M-enk-like substance (MELS) was present in blood and urine in normal subjects, but not L-enk-like substance (LELS). Plasma MELS and its urinary output averaged 38 +/- 14 pg/ml (N = 19) and 605 +/- 235 ng/day (N = 15, M. +/- S.D.), respectively. There was a significant increase in plasma MELS and its urinary output in patients with pheochromocytoma. Plasma MELS did not show any significant increase or decrease in Cushing's disease. Addison's disease, panhypopituitarism or chronic glomerulonephritis. The urinary output of MELS was significantly increased in patients with essential hypertension, renovascular hypertension and primary aldosteronism, but was decreased in central diabetes insipidus.
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PMID:The presence of methionine-enkephalin in plasma and urine in normal human subjects and various patients. 408 13

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

In a previous study we observed an increase in urinary cyclic AMP in labile hypertension in the upright position and during isoproterenol infusion, in contrast to a decrease in control subjects. In the present study we measured the plasma level of cyclic AMP in control subjects and patients with various types of hypertension. We obtained the following results: (1) plasma cyclic AMP increases in response to upright posture in control subjects and hypertensive patients; (2) values of cyclic AMP in the recumbent and upright positions are comparable in control subjects and patients with essential hypertension, but are significantly higher in those with true renovascular hypertension due to bilateral renal artery stenosis; (3) propranolol inhibits the increase of plasma cyclic AMP in response to posture in control subjects, but has an opposite effect in labile hypertension where there is a further increase; (4) the rise in blood pressure in pheochromocytoma is associated with a considerable increase in plasma cyclic AMP.Present and previous data suggest that kidney handling of cyclic AMP is abnormal in hypertension, and that the specific defect may be related to the type of hypertension.
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PMID:Plasma adenosine 3',5'-cyclic monophosphate in human hypertension. 436 18

The metabolic fate of the tyrosine hydroxylase inhibitor, alpha-methyl-para-tyrosine (alpha-MPT), was studied after oral administration of single and multiple doses to patients with pheochromocytoma and essential hypertension. No major urinary excretion product was found other than the drug itself, which accounted for 44-88% of the fate of single or repeated oral doses. Though less than 1% of the administered drug could be recovered in the urine as catechol metabolites, it was possible to identify alpha-methyldopa, alpha-methyldopamine, and alpha-methylnorepinephrine and to quantify the excretion of the first two of these compounds. This minor route of metabolism required revision of methodology (presented herein) for measuring urinary catecholamines during alpha-MPT treatment since these compounds produce spurious fluorescence in routine methods of assay for catecholamines. The catechol metabolites probably are not present in sufficient amounts to contribute to the biochemical effects of the drug. Determination of plasma concentrations of alpha-MPT during maintenance therapy and considerations of the kinetics of enzyme inhibition enabled a calculation to be made of the degree of inhibition of catecholamine synthesis to be expected in the patient. This was calculated to be about 75% for the highest doses employed and is similar in magnitude to experimentally determined values.
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PMID:Metabolism of alpha-methyltyrosine in man: relationship to its potency as an inhibitor of catecholamine biosynthesis. 563 44

Alpha methyltyrosine (alpha-MPT) was administered to 52 patients from 4 days to 10 months; 22 patients were cases of pheochromocytoma and 20 had essential hypertension. Inhibition of catecholamine synthesis in the range of 50-80% was achieved with divided daily drug dosage of from 1.0 to 4.0 g. Striking clinical benefit was noted in patients with pheochromocytoma in whom the drug was used in preparation for surgery and during chronic medical management. The drug appeared to have limited usefulness when used in essential hypertension, unless added to existing therapy with conventional agents. No beneficial effects were noted in thyrotoxicosis, glaucoma, and Raynaud's phenomenon. Untoward effects in order of decreasing incidence were: sedation (with insomnia on withdrawal), anxiety, tremor, diarrhea, and galactorrhea. Drug crystalluria, which has been observed in animals and is currently restrictive of clinical trials, was not observed in these studies. Evidence is presented that the minor conversion of alpha-MPT to methyldopa probably does not contribute significantly to the central and peripheral effects of the drug.
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PMID:Biochemical and pharmacologic effects of alpha-methyltyrosine in man. 563 45

A radioimmunoassay involving an 125I ligand has been developed and applied to the measurement of urinary metanephrine. To validate the clinical usefulness of this assay, we compared measurement of metanephrine by radioimmunoassay and of total urinary metanephrines by the Pisano colorimetric method. The radioimmunoassay is specific for metanephrine, whereas the colorimetric method measures both metanephrine and normetanephrine. We used both methods to determine urinary metanephrine or total metanephrines in subjects with essential hypertension, pheochromocytoma, the syndrome of multiple endocrine adenomatosis type 2, and normotensive volunteers. The mean and upper limit of normal (3 SD) for metanephrine by radioimmunoassay in our normotensive volunteers was 94.2 microgram/24 h and 229 microgram/24 h, respectively, which compares well with reported values of 87.6 microgram/24 h and 319 microgram/24 h by non-radioimmunoassay methods. Both radioimmunoassay and colorimetry accurately identified five patients with known pheochromocytoma. Good correlation (r = 0.993) was demonstrated between the two assays in a comparison of patients with essential hypertension and pheochromocytoma. We conclude that the radioimmunoassay is at least equivalent to the colorimetric methods in distinguishing pathological and normal catecholamine secretion, and is faster, more precise, and 1000-fold more sensitive.
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PMID:Urinary metanephrine radioimmunoassay: comparison with the colorimetric assay. 610 4

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

Fifteen patients with essential hypertension and ten with pheochromocytoma were studied to assess the effect of clonidine, a centrally acting antihypertensive agent, on the functional and biochemical indices of sympathetic function. Single oral doses of clonidine (0.3 mg) decreased supine plasma norepinephrine significantly in essential hypertension, but not in pheochromocytoma despite producing similar reductions in blood pressure and heart rate. Plasma renin activity was unchanged in both groups. In untreated essential hypertension, head-up tilt increased diastolic blood pressure, heart rate, and plasma norepinephrine. Three hours after a single oral dose of clonidine, head-up tilt resulted in significant blood pressure reductions, although heart rate and plasma norepinephrine increased dramatically. Clonidine might reduce blood pressure by inhibiting sympathetic outflow, and any effect on plasma renin activity appears unimportant in its antihypertensive action. In pheochromocytoma clonidine decreases blood pressure without altering plasma norepinephrine, which is consistent with the concept that the norepinephrine released from axon terminals of sympathetic postganglionic neurons is biologically more significant than circulating catecholamines.
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PMID:Effects of clonidine on sympathetic function. 633 29


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