Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension is a well-known finding in some patients with neuroblastoma. However, it has not previously been described in association with the use of Imipramine. We report the occurrence of severe hypertension (blood pressure 190/160) in a 4-year-old girl with neuroblastoma who was given Imipramine to control a behavior disorder. It was determined later that this patient's tumor was recurring at the time of her hypertensive episode. Since she had no blood pressure elevation at initial diagnosis and none following discontinuation of the Imipramine (when she was in florid relapse), we believe that this drug rather than her underlying disease alone caused her hypertension. The mechanism for this reaction is believed to be increased levels of vasoactive catecholamines due to interference of their physiologic inactivation by Imipramine. From this experience, we urge extreme caution in the use of tricyclic antidepressants in children with active neuroblastoma.
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PMID:Hypertension in neuroblastoma induced by imipramine. 343 80

We report a case of bilateral papilloedema in an adult male with neuroblastoma, in the absence of hypertension or detectable intracranial disease. This complication has not previously been described in the English-speaking literature. Possible mechanisms are discussed.
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PMID:Paraneoplastic papilloedema in neuroblastoma. 344 13

A 2 1/2 year old dystrophic girl with polyuria and polydipsia was found to have an arterial hypertension, increased catecholamines in serum and urine, and a suprarenal tumour was diagnosed by ultrasonic scan. By means of histology and staging a neuroblastoma grade 3 was revealed. The sonography and Iodine-benzyl-guadinin-scintigraphy gave the clearest information about the tumour. Before operating it is necessary to stabilize the blood pressure at a normal level with alpha and beta blocking substances, in order to reduce the risk of an intraoperative hypertonic crisis and a vasodilative shock after tumour extirpation.
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PMID:[Differential diagnostic and therapeutic problems in a neuroblastoma patient with hypertension]. 352 13

The presence of angiotensinogen messenger RNA (mRNA) was assessed in total RNA extracted from hepatoma, glioma, neuroblastoma, and glioma-neuroblastoma hybrid cell lines. Total RNA from 1 X 10(7) cells was extracted, transferred to a membrane, and hybridized with a 32P-labeled, full-length (1650-base pair) rat angiotensinogen complementary DNA (cDNA). Angiotensinogen RNA sequences could be definitively detected only in hepatoma cells. Steroids were used in an attempt to increase the angiotensinogen mRNA level. Dexamethasone (2 X 10(-6) M) or 17 beta-estradiol (1 X 10(-7) M) was added to the cultures 18 to 24 hours prior to harvest. Dexamethasone treatment of the hepatoma cells resulted in a large increase in angiotensinogen mRNA, whereas estradiol had no effect. Steroids failed to induce detectable levels of angiotensinogen mRNA in total RNA from the other cell lines. That the RNA was intact was ensured by hybridizing duplicate Northern blots to a 32P-labeled actin cDNA. Actin mRNA sequences were detected in all cell lines. Blot hybridization of poly(A)+RNA resulted in the visualization of a weak angiotensinogen mRNA signal for a glioma cell line and a glioma-neuroblastoma hybrid line. However, the ability to detect angiotensinogen mRNA in a cell may depend on the phenotype expressed, which can be governed by culture conditions.
Hypertension 1987 Jun
PMID:Presence of angiotensinogen messenger RNA in various cultured cell lines. 359 87

The murine IgG3 monoclonal antibody (MoAb) 3F8, specific for the ganglioside GD2, activates human complement, is active in antibody-dependent cell-mediated cytotoxicity (ADCC), and can target specifically to human neuroblastoma in patients with metastatic disease. In a phase I study, 3F8 was administered intravenously (IV) to 17 patients with metastatic GD2 positive neuroblastoma or malignant melanoma at doses of 5, 20, 50, and 100 mg/m2. Serum 3F8 levels achieved were proportional to the dose of 3F8 infused. However, serum antimouse antibody levels did not increase with the amount of 3F8 administered. Toxicities included pain, hypertension, urticaria, and complement depletion. All acute side effects were controllable with symptomatic therapy. No long-term side effects were detected in patients observed for more than 14 months. None of the 17 patients received any antitumor therapy postantibody treatment. Antitumor responses occurred in seven of 17 patients. These ranged from complete clinical remissions to mixed responses. The murine monoclonal antibody (MoAb) 3F8 has clinical utility for the diagnosis and therapy of neuroblastoma and melanoma.
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PMID:Ganglioside GD2 specific monoclonal antibody 3F8: a phase I study in patients with neuroblastoma and malignant melanoma. 154 29

Autonomic dysreflexia and catecholamine secreting tumor, each of which causes paroxysmal hypertension, coexisted in a young man. Two years after neuroblastoma was diagnosed, he developed T4 incomplete paraplegia due to metastases to the spine at T5 and L3 levels. Shortly after the onset of paraplegia, paroxysmal hypertension developed. The hypertension was controlled adequately by good bowel and bladder management and oral clonidine. The paroxysmal hypertension is believed to have resulted from the synergistic effect of the high levels of circulating catecholamines from the tumor and the disruption of autonomic pathways.
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PMID:Autonomic dysreflexia in a paraplegic man with catecholamine-secreting neuroblastoma. 374 Oct 83

A 28-year-old man with the chronic syndrome of Inappropriate antidiuretic hormone secretion and hypertension was found to have an olfactory neuroblastoma. We demonstrated evidence of elevated circulating arginine vasopressin levels, significantly elevated arginine vasopressin and vasopressin neurophysin levels in the tumor extract, and immunohistochemical staining for arginine vasopressin and vasopressin neurophysin in the tumor cells. The patient's clinical syndrome, including hypertension, resolved following subtotal removal of the tumor and radiation therapy. This study identified olfactory neuroblastoma as a definite cause of ectopic arginine vasopressin secretion causing the syndrome of inappropriate antidiuretic hormone secretion.
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PMID:Chronic syndrome of inappropriate antidiuretic hormone secretion and hypertension in a patient with olfactory neuroblastoma. Evidence of ectopic production of arginine vasopressin by the tumor. 375 13

Stenosis of the renal artery secondary to an extrinsic acquired compression of the renal artery because of a tumor is rare. We report two cases. The first case is a boy of 14 months with a large neurogenic tumor from the right renal plexus with compression of the right renal artery. The second case is a girl of 2 years which had a neuroblastoma displacing the right kidney. The right renal vessels were invaded by very calcified solid masses and the removal was very difficult. Arterial hypertension secondary to an acquired unilateral renal stenosis may be healed definitely thanks to surgery.
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PMID:[Arterial hypertension caused by extrinsic compression of the renal artery of tumor origin in a child]. 380 50

In a series of 11 cases with phaeochromocytoma, two patients were found in whom the tumour secreted dopa in addition to dopamine, noradrenaline, and adrenaline. These two patients were normotensive in spite of high plasma and urinary levels of noradrenaline and adrenaline. This raises the possibility that dopa may be able to protect against the hypertensive action of noradrenaline. Such a mechanism would also explain the absence of hypertension in many cases of neuroblastoma.
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PMID:Secretion of dopa in phaeochromocytoma. 463 12

Twenty years ago it was demonstrated that angiotensin II (Ang II) acts on the brain, which results in an elevation of blood pressure. Ten years later, reninlike activity was discovered in the brain of the rat and dog, which gave rise to the concept of an endogenous brain renin-angiotensin system. In the periphery, the kidney, liver, and lungs work in unison to produce Ang II. Evidence for brain renin, substrate, converting enzyme, and angiotensins is reviewed. New data indicate that the enzyme system for the synthesis of Ang II within the brain may in fact be contained in the cell. All the components for a renin-angiotensin system have now been found in neuroblastoma/glioma cell lines and Ang II is present in primary cell culture of rat brain neurons. The significance of angiotensin in the brain for hypertension is that it may be a stimulus for vasopressin release and sympathetic activation, which can maintain high blood pressure. In the spontaneously hypertensive rat, there is evidence of increased brain angiotensin. Also, experiments with angiotensin-converting enzyme inhibitors show that blockade of brain angiotensin production leads to a long-lasting lowering of blood pressure. The activity of the inhibitors in part appears to be directly on the brain.
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PMID:New evidence for brain angiotensin and for its role in hypertension. 630 29


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