Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pituitaries and adrenals of 30 patients died from extensive fresh myocardial infarction and of 25 patients died from other diseases were studied. In myocardial infarction the mean weight of the above glands was significantly higher than in other diseases. In most cases an increase in number of pituitary ACTH-cells was observed with the immunoperoxidase method. In non-cardiogenic shock (another 9 cases) gland weight was also increased but without a significant increase in the number of ACTH-cells. Hyperactivity of the anterior pituitary-adrenal system is due to a number of known factors. It may be assumed that patients who have infarction are either exposed to an extraordinary amount of stress stimuli or are more susceptible to stress than normal subjects. The findings may indicate the morphological basis of this situation. Of the shock phenomena, incomplete necrosis and haemorrhage of the adrenal cortex are frequent. In the pituitary neural lobe the neurosecretory material, which proved to be vasopressin with the PAP-method, was found to be increased more frequently in myocardial infarction than after other diseases.
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PMID:Immunocytochemical investigation of ACTH-cells and vasopressin in the pituitaries of humans died from myocardial infarction. 303 36

Since current data on vasopressin (AVP) secretion during the early phase of myocardial infarction is not extensive, plasma AVP was measured in 26 patients with acute myocardial infarction. Twelve had an increased AVP concentration (23.2 +/- 7.0 pg/ml; mean +/- SEM) whereas 14 had an AVP level less than 3 pg/ml (1.96 +/- 0.14 pg/ml). The patients with AVP greater than 3 pg/ml had higher heart rate and plasma osmolality than those with AVP less than 3 pg/ml. Blood pressure values were the same in both groups of patients. There was no difference in peak CPK and iso CPK activities between the two groups. Seven patients with AVP greater than 3 pg/ml died within the next few days, while only 1 patient with AVP less than pg/ml died. It thus appears that increased AVP concentration during acute myocardial infarction is associated with a poor prognosis. Whether it is a cause or a consequence of an unfavourable course of myocardial infarction remains to be determined.
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PMID:[Vasopressin in acute myocardial infarct: clinical implications]. 381 98

A patient exhibited brain damage, polyuria, and refractory hypernatremia after myocardial infarction and cardiopulmonary arrest. Serum vasopressin levels were relatively fixed and inappropriately low for the elevated serum osmolality. Hypernatremia persisted despite administration of vasopressin; after vasopressin was discontinued, serum sodium value was corrected with small doses of furosemide and replacement of free water. In her case, impairment of osmotic homeostasis could not be attributed to either simple resetting or complete destruction of osmoreceptors; metabolic normalization required an unusual therapeutic approach.
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PMID:Polyuria and refractory hypernatremia after cardiopulmonary arrest. 381 34

Earlier we have shown in the dog model mimicking angina on effort a delayed antiischaemic effect of PgI2 and its stable analogue 7-oxo-PgI2-Na, appearing only when the drug induced marked vasodilatation was over [1]. In the present experiments we could show that the protective effect appears at a time when the blood pressure returned to normal and in addition the marked platelet aggregation inhibitory effect has also faded away. In the rat 7-oxo-PgI2 could substantially diminish vasopressine induced T-wave elevation in the ECG if given 2 hours before administration of vasopressin. In addition it could moderate the vasopressin induced metabolic changes appearing as diminution of the myocardial CP and ATP-level and increase of the myocardial lactate content. A similar metabolic protection was found in the heart of rats pretreated with 7-oxo-PgI2 2 hours before taking myocardial samples and exposing them for 1 minute to ischaemia by incubation in Ringer solution. It is concluded that a direct metabolic and hemodynamic effect could be at least partly responsible for the late antiischaemic effect of 7-oxo-PgI2. This effect was also present in the early phase of experimental myocardial infarction in conscious rats if animals were pretreated with 7-oxo-PgI2 2 hours before occlusion. However treatment did not increase survival rate and failed to reduce the incidence and severity of arrhythmias.
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PMID:On the late antiischaemic action of the stable PgI2 analogue: 7-oxo-PgI2-Na and its possible mode of action. 639 60

Tobacco smoking increases the risk of myocardial infarction and sudden death. When used for diagnostic and therapeutic ends, vasopressin, at low doses, may induce acute ischaemic complications in patients with coronary artery disease. This study showed that in some patients the inhalation of tobacco smoke caused a rise in plasma vasopressin and nicotine-stimulated-neurophysin, a substance easily measured and used as a marker of vasopressin secretion because of the close relationship of the two substances. Twelve out of twenty five subjects presented higher levels of nicotine-stimulated-neurophysin than the normal for the same group before smoking (p less than 0,005): 280 +/- 54 compared to 714 +/- 459 pg/ml. Simultaneous measurement of vasopressin and nicotine-stimulated-neurophysin every 5 minutes in 4 subjects confirmed the parallel changes of these substances during smoking. These results suggest that vasopressin may play a primary role in the acute ischaemic complications of tobacco smoking. The concept of the "vasopressin response" could be used as a biological parameter to identify subjects at "high cardiovascular risk" under the effects of tobacco and so lead to a prophylactic strategy aimed more specifically at these patients.
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PMID:[Possible role of vasopressin in ischemic accidents related to tobacco consumption]. 642 96

[(5Z,13E,9 alpha,11 alpha,15S)-2,3,4-Trinor - 1,5 - inter-m - phenylene - 6,9 - epoxy - 11,5 - dihydroxy - 15 - cyclohexyl - 16,17,18,19,20-pentanor]- prosta-5,13-dienoic acid (sodium salt) (CG 4203) is a new stable epoprostenol (prostacyclin) analogue with a relative platelet antiaggregatory potency of 0.46 (ADP aggregation in vitro) and a hypotensive potency of 0.14 (anaesthetized rat i.v.) as compared to epoprostenol. In isolated perfused rat hearts, CG 4203 (4.64 X 10(-9) mol/l) significantly attenuated arrhythmias and loss of left ventricular creatine kinase (CK) activity observed in control hearts after 30 min perfusion with hypoxic and 30 min reperfusion with oxygenated Krebs-Ringer solution. In anaesthetized rats, CG 4203 (1.0 microgram X kg-1 X min-1 i.v.) significantly reduced incidence of ventricular fibrillation and increase in plasma CK activity after ligation of the left coronary artery. Infusion of 1.0 and 2.15 micrograms X kg-1 X min-1 CG 4203 i.v. in anaesthetized rats dose-dependently inhibited electrocardiographic changes, i.e. ST depression observed after i.v. injection of 1.0 IU X kg-1 vasopressin. In rat models of sustained myocardial hypoxia, myocardial infarction, and transient cardiac ischemia, CG 4203 thus exerts cardioprotective effects which, depending on the model considered, may be ascribed to either its vasodilatory, coronary dilatory, antiaggregatory or epoprostenol-like cytoprotective activity.
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PMID:Cardioprotective action of the new stable epoprostenol analogue CG 4203 in rat models of cardiac hypoxia and ischemia. 644 79

The role of antidiuretic hormone (ADH) in the pathogenesis of renal impaired water excretion in acute respiratory failure has not been clearly delineated. Plasma sodium concentration and plasma ADH levels (radioimmunoassay) were therefore serially measured in 13 patients with acute respiratory failure (10 with acute exacerbations of chronic lung disease and three with acute lung disease) and eight "control" patients admitted ot the intensive care unit with suspected myocardial infarction. None of the patients had systemic hemodynamic, hepatic or renal dysfunction. ADH levels were significantly elevated in patients with acute respiratory failure (15.1 +/- 5.2 pg/ml versus 5.7 +/- 1.9 pg/ml, p less than 0.05) when compared with levels in control patients. The elevated ADH levels occurred despite significantly lower plasma sodium concentration (133 +/- 1 meq/liter versus 138 +/- 2 meq/liter, p less than 0.05) compared wit control values. Moreover, markedly increased ADH values (range 1.1 to 13.0 pg/ml) were often encountered in patients with acute respiratory failure despite significant hyposmolality (263 to 275 mOsm/kg H2O). This was not observed in any control patients. These results suggest that patients with acute respiratory failure are susceptible to water retention and hyposmolality due to nonosmotic release of antidiuretic hormone.
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PMID:Plasma antidiuretic hormone in acute respiratory failure. 707 43

In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. Neurological deterioration was reversed in 47 patients, transiently in 4; permanent improvement occurred in 43. Complications experienced during therapy included pulmonary edema, dilutional hyponatremia, aneurysmal rebleeding, coagulopathy, hemothorax, and myocardial infarction. Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.
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PMID:Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. 713 49

Several controlled studies with the best methodology had showed that digoxin improves the symptoms of patients with chronic heart failure and sinus rhythm, whose ventricular systolic function is impaired. The Proved and Radiance studies show that in patients receiving diuretics and digoxin, or angiotensin-converting enzyme (ACE) inhibitors, diuretics and digoxin, the withdrawal of digoxin results in clinical deterioration and worsening of exercise tolerance. In addition to an inotropic action, digitalis exerts effects in the neurocardiovascular axis, produces reduction in plasma norepinephrine, renin, aldosterone, vasopressin activity and restores a more normal sympathetic-parasympathetic autonomic balance and baroreceptor function. ACE inhibitors reduce mortality, improve symptoms and exercise tolerance in patients with chronic heart failure in class IV (Consensus I trial), in class II and III (SOLVD, treatment trial) and prevent the development of heart failure in asymptomatic patients with ejection fraction < 35% (SOLVD, prevention trial). When ACE inhibitors are administered per os, more than 3 days after acute myocardial infarction they reduce mortality, severe heart failure, re-hospitalization, and induce an unexpected reduction of recurrent myocardial infarction (SAVE trial). However, the early administration, within 2 hours after the onset of chest pain, of ACE inhibitors by intravenous infusion, does not improve survival; the hypotension may be responsible of increased mortality (Consensus II trial).
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PMID:[Digoxin and angiotensin-converting enzyme inhibitors in the treatment of chronic congestive heart failure]. 787 86

The purpose of this study was to investigate whether neurohumoral activation occurs in asymptomatic patients with acute myocardial infarction (AMI) and without clinical signs of heart failure. During the early phase of AMI (mean 8 days), the neurohumoral profiles of 60 patients (mean age 59 range 37 to 70) were examined. Blood levels of the following humoral parameters were measured: atrial natriuretic peptide (ANP), plasma renin activity, aldosterone and vasopressin. All patients underwent cardiac catheterization during hospitalization. Baseline hemodynamic characteristics identified left ventricular dysfunction (ejection fraction < or = 45% and/or left ventricular end-diastolic pressure > or = 15 mmHg) in 32 patients; the remaining 28 patients had normal hemodynamic parameters. In patients with AMI, plasma ANP levels differed significantly from control subjects (111 +/- 74 pg/ml vs. 53 +/- 18 pg/ml; P < 0.001). In patients with AMI and mild left ventricular dysfunction ANP levels were significantly increased when compared to patients with AMI and normal left ventricular function (129 +/- 73 pg/ml vs. 82 +/- 69 pg/ml; P < 0.001). The hemodynamic data showed a significant correlation with ANP only in patients with AMI and left ventricular dysfunction (EF% r = 0.42; LVEDP r = 0.44; P < 0.001). These data show that in patients with myocardial infarction and without heart failure, the atrial natriuretic peptide is the only neurohumoral system activated out of all neurohumoral systems tested in this population and its circulating levels are strictly related to the degree of left ventricular dysfunction.
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PMID:Selective activation of atrial natriuretic peptide in patients with myocardial infarction and mild left ventricular dysfunction. 811 15


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