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)

Five patients received overdoses of vincristine ranging from 3.5 to 32 mg. Neurotoxicity accounted for most of the complications observed. Peripheral neuropathies, cranial nerve palsies, paralytic ileus, atony of the bladder, hypertension, hypotension, seizures, inappropriate ADH secretion, and severe bone marrow depression were all encountered. Two patients died within 72 hours of the overdose. Another patient died of sepsis 22 days after the overdose. Two patients recovered and were discharged. The three patients who survived longer than a few days showed improvement in the vincristine-induced neuropathy, and the two long-term survivors had essentially complete recovery. It appears that if a patient can be supported through the critical period following an overdose, he can be expected to recover normal neurologic function.
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PMID:Overdosage with vincristine. 18 48

1. Evidence from numerous experiments incorporating central blood volume expansion and changes in sodium status supports atrial stretch as the prime determinant of ANF release. 2. Plasma ANF levels are the result of both secretion and clearance of the peptide. Clearance is altered by a number of factors, including changes in posture in normal man and is probably impaired in disease states with diminished renal and hepatic blood flow. 3. In normal subjects an inverse relationship exists between plasma ANF values and renin-angiotensin-aldosterone system activity. This relationship is lost and replaced by a positive association in heart failure, presumably reflecting the abnormal concurrence of increased atrial stretch and diminished renal perfusion in this condition. Plasma ANF values rise with increasing severity of heart failure and fall with effective treatment. 4. Plasma ANF values are elevated in hypertension and cardiac tachyarrhythmias possibly reflecting raised central venous and atrial pressures. 5. A variety of other disorders may be associated with abnormal plasma ANF values including cirrhosis and the syndrome of inappropriate ADH secretion. 6. Evidence from low-dose infusions of ANF in normal volunteers suggests that the variations in plasma ANF seen in health and disease are sufficient to exert biological effects. 7. The advent of a specific antagonist is needed to provide further insight into the physiological and pathophysiological roles of ANF.
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PMID:Atrial natriuretic factor in human pathophysiology. 297 38

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

A 13-year-old girl with multiple minor anomalies and severe mental retardation had recurrent episodes of severe vomiting. At each episode, marked elevations of plasma ADH, ACTH, cortisol and salivary type amylase were found with reduction of serum Na level and osmolarity. This case is similar to that with periodic ACTH-ADH discharge syndrome (Sato). However, she had underlying disease, and neither hypertension nor depressive state was observed. Latent SIADH was detected by water loading test. After DZP administration, ADH secretion was suppressed in this test, and actually the duration of each attack was shortened. We considered that her vomiting was closely related with hypothalamic dysfunction, especially latent SIADH.
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PMID:[Congenital multiple anomaly syndrome with recurrent vomiting accompanied with latent SIADH; a case report]. 828 Apr 47

A 65-year-old man visited our hospital with complaints of tingling sensation in the distal parts of his extremities and dysuria, which first appeared 2 months before admission. He had no abnormal findings on physical examination. Neurological examination revealed sensory impairment of glove and stocking type, mild motor weakness and muscular atrophy in the proximal parts of arms and legs, and absent tendon reflexes in knees and ankles. Fasciculation was observed on his shoulders and upper extremities, and myokymia on the abdominal wall and bilateral calves. He had hyponatremia, which was proved to be caused by SIADH. Anti-acetylcholine receptor antibody, anti-GM1 ganglioside antibody and anti-galactocerebroside antibody were detected in the serum. Chest X-ray showed mass shadows in the mediastinum, which were confirmed as malignant thymoma by needle biopsy. Orthostatic hypotension, neurogenic bladder and anhidrosis were observed by the autonomic function tests. Lesions responsible for orthostatic hypotension and SIADH were suspected in the afferent fibers from baroreceptors, since an reactive increase of plasma arginine vasopressin to orthostatic hypotension was blunted and reflex hypertension in the cold pressor test was well-preserved, while overshoot in Valsalva's maneuver was absent. It is important that afferent baroreceptor dysfunction may be associated with paraneoplastic neurological syndrome, since lesions in acute autonomic neuropathy are usually in the efferent fibers.
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PMID:[A case of paraneoplastic autonomic and sensorimotor neuropathy with dysfunction in the afferent limb of baroreflex arc]. 840 86

A 69-year-old woman with a history of diabetes and hypertension, was referred to the Hospital of Laredo because of hyponatraemia. She had weakness and slight dyspnoea with no evidence of extracellular fluid volume depletion or oedema. Serum sodium level on admission was 125 mol l-1, plasma osmolality 270 mosmol kg-1, simultaneous urine osmolality was 580 mosmol kg-1 and urine sodium 32.6 mmol l-1. She had been treated with enalapril (20 mg) daily for 4 months. She was diagnosed with the Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) that was reversed after cessation of treatment with enalapril and reappeared on reintroduction of the drug at the same daily doses.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and enalapril. 832 83

Plasma osmolality normally decreases in early pregnancy, reaching a minimum at approximately 10 weeks and remaining depressed until term. This is associated with a mean decrease of 4 mEq/L in the plasma sodium level, and with an altered threshold for arginine vasopressin (AVP) release and for thirst. We describe a patient who developed more severe hyponatremia (120 mEq/L), which accompanied the development of hypertension and edema at 37 weeks in her fourth pregnancy. Hyponatremia and hypo-osmolality were associated with marked elevation of the plasma AVP level. The hyponatremia and elevated AVP level resolved after the delivery of the infant. To our knowledge, this is the first reported example of transient inappropriate antidiuretic hormone secretion (SIADH) associated with pregnancy.
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PMID:Transient syndrome of inappropriate antidiuretic hormone secretion during pregnancy. 846 26

We studied seizures that occur during the acute phase of aseptic and bacterial meningitis in childhood. Of the 108 children with aseptic meningitis, five had seizures (4.7%). Four patients developed them within 24 hours of the onset of the initial symptom (fever in 3 cases), and three had repeated seizures on the first day. One case had SIADH complication, but another neurologic abnormalities were not observed. On the 18 children with bacterial meningitis, three cases (16.7%) had seizure, which occurred on the second day of illness. Disturbance of consciousness and cerebral hypertension were observed in 2 cases each, and abnormal cerebral CT findings in all the three. The NSE level in the cerebrospinal fluid was elevated in 2 cases. Thus, seizures occurring in the acute phase of aseptic meningitis may reflect transient cerebral functional abnormality accompanying fever or SIADH, whereas those in bacterial meningitis may result from neural tissue damage due to encephalopathy or angitis. In aseptic and bacterial meningitis, the presence of seizures in the acute phase was not correlated with the neurological outcome.
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PMID:[Seizures in the acute phase of aseptic and bacterial meningitis]. 984 13

After the story of success of hormone blockers for catecholamines, aldosterone and angiotensin II and their successful implementation into clinical practice another endocrine cardiovascular system has come into focus. It has long been known, that the hormone vasopressin plays an important role in peripheral vasoconstriction, hypertension and in several disease conditions with dilutional hyponatremia in edematous disorders, like congestive heart failure, liver cirrhosis, SIADH and nephrotic syndrome. A series of orally active nonpeptide antagonists against the vasopressin receptor subtypes has recently been synthesized and is now under intensive examination. Nonpeptide V1a-receptor specific antagonists, OPC 21268 and SR 49059, nonpeptide V2-receptor specific antagonists, SR 121463 A and VPA 985, and combined V1a-/V2-receptor antagonists, OPC 31260 and YM 087, have become available for clinical research. AVP-V2-receptor antagonists lead to a dose-dependent diabetes insipidus in animals and man. The term aquaretic drugs (aquaretics) has been coined for these drugs to highlight their different mechanism compared to the saluretic diuretic furosemide. V1a-receptor antagonists might offer new therapeutic advantages in the treatment of vasoconstriction and hypertension. Combined V1a-/V2-receptor antagonists might be beneficial in the treatment of congestive heart failure. Early results are promising and now need to be confirmed in large clinical studies.
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PMID:Nonpeptide vasopressin antagonists: a new group of hormone blockers entering the scene. 1037 39

Vasopressin (AVP) is a cyclic nonapeptide hormone that exhibits many physiological effects including free water reabsorption, vasoconstriction, cellular proliferation and adrenocorticotrophic hormone (ACTH) secretion. In a healthy organism, AVP plays an important role in the homeostasis of fluid osmolality and volume status. However, in several diseases or conditions such as the syndrome of inappropriate secretion of AVP (SIADH), congestive heart failure, arterial hypertension, liver cirrhosis, nephrotic syndrome, dysmenorrhoea and ocular hypertension, AVP may play an important role in their pathophysiology. Recently, orally-active non-peptide AVP receptor antagonists were developed by random screening of chemical entities and optimisation of lead compounds. These include agents specific for the V(1)-vascular and V(2)-renal AVP receptor subtypes. Dual V(1)/V(2) AVP receptor antagonists are also being studied. Some of these non-peptide receptor antagonists have been studied extensively, while others are currently under investigation. Potential therapeutic indications for AVP receptor antagonists comprise: 1) The blockade of V(1)-vascular AVP receptors in arterial hypertension, congestive heart failure, Raynaud's syndrome, peripheral vascular disease and dysmenorrhea. 2) The blockade of V(2)-renal AVP receptors in the syndrome of inappropriate secretion of vasopressin, congestive hart failure, liver cirrhosis, nephrotic syndrome and any state of excessive retention of free water and subsequent dilutional hyponatraemia. 3) The blockade of V(3)-pituitary AVP receptors in ACTH-secreting tumours. This review examines the pharmacology of orally-active non-peptide AVP receptor antagonists and their clinical applications.
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PMID:Development and therapeutic indications of orally-active non-peptide vasopressin receptor antagonists. 1132 60


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